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Slyvka, N. O. "Systemic inflammatory response as a part of hepatorenal syndrome". Thesis, БДМУ, 2020. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18059.
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Chen, Xu-wu. "Neutrophil-endothelium interactions in patients with systemic inflammatory response syndrome". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ29673.pdf.
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Chen, Xu-wu 1955. "Neutrophil-endothelium interactions in patients with systemic inflammatory response syndrome". Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=27298.
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Multiple Organ Dysfunction Syndrome (MODS) is associated with high mortality in patients admitted to the surgical intensive care unit (SICU). MODS begins with a systemic response described as Systemic Inflammatory Response Syndrome (SIRS). Studies on SIRS patients may provide an insight into the mechanisms by which SIRS progresses to MODS. In this thesis, the interactions between circulating polymorphonuclear neutrophils (PMNs) from patients with SIRS and endothelial cells (ECs) from human umbilical veins were measured in order to elucidate the mechanism for PMN adhesion and subsequent cytotoxicity of the ECs. PMNs from patients with SIRS were compared to PMNs from pre-operative surgical patients without SIRS and with healthy control subjects, in vitro. The results showed that PMNs adherence to ECs increased progressively from healthy controls to patients with SIRS. PMN-HUVE cytotoxicity, however, did not show this trend. PMNs from SIRS patients treated with lipopolysaccharide, unlike PMNs from patients without SIRS or healthy controls, showed no increase in PMN-EC adhesion. The results also showed that EC activation with TNF-$ alpha$ and Il-1$ beta$ led to high levels of PMN-EC adhesion and cytotoxicity, whereas PMN treatment with lipopolysaccharide played a lesser role. Autologous plasma provided significant protection from PMN mediated EC damage. From this data I conclude that activation of the EC by cytokines associated with SIRS is far more important in promoting PMN-EC adhesion and subsequent cytotoxicity than PMN stimulation with lipopolysaccharide and that there are host factors in plasma that modulate this response.
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Sydorchuk, Ryslan Ihorovuch, Oleg Yosypovych Khomko, Ruslan Ihorovych Polyanskyi e Oleksandr Matviyovych Plegutsa. "Systemic inflammatory response syndrome associated with pancreatitis: efficacy of passive immunotherapy". Thesis, Вінницький національний медичний університет ім. М.І.Пирогова, 2015. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/10764.
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Price, Susanna. "Role of vasoactive mediators in the modulation of cardiac function in sepsis". Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271284.
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Pevec, Till. "Dexamethason-21-isonicotinat als Begleittherapie bei Kühen mit Systemic Inflammatory Response Syndrome". Doctoral thesis, Universitätsbibliothek Leipzig, 2007. http://nbn-resolving.de/urn:nbn:de:bsz:15-20071210-143013-1.
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Dexamethason-21-isonicotinat als Begleittherapie bei Kühen mit Systemic Inflammatory Response Syndrome Schlüsselwörter: Dexamethason, SIRS, Phagozytoseaktivität/Burstaktivität von Monozyten und neutrophilen Granulozyten, Tumornekrose Faktor alpha
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Keyser, Eric J. "Exhaled nitric oxide and the Systemic Inflammatory Response Syndrome (SIRS) after cardiac surgery". Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=31247.
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Background. Septic patients produce increased nitric oxide (NO). We postulated increased exhaled nitric oxide (exNO) in SIRS after cardiopulmonary bypass surgery (CPB).Methods. Forty-two intubated patients were studied postoperatively and at two-hour intervals for eight hours or until extubated. Hemodynamic indices, including indexed systemic vascular resistance (SVRi) and cardiac index (CI) were measured. ExNO was analyzed by ozone chemiluminescence.
Results. Six patients (14%) Manifested SIRS, defined as SVRI <1800 dynes·sec/cm5/m2. ExNO indexed by expired volume of minute ventilation and body surface area (exNO· V˙Ei) was less in SIRS patients at each interval. Overall, normal exNO·V˙Ei was 4.3 +/- 0.4 nL/min/m2 with a Cl of 2.56 +/- 0.05 L/min/m 2 and an SVRI of 2488 +/- 62 dynes·sec/cm5/m 2, whereas in SIRS exNO·V˙Ei was 0.7 +/- 0.3 (p < 0.001) with a Cl of 2.97 +/- 0.09 (p < 0.001) and an SVRi of 1826 +/- 86 (p < 0.001).
Conclusions. Pulmonary production of NO in post-CPB SIRS differs from sepsis and may not be reflective of systemic levels. Increased pulmonary blood flow may scavenge lung production of NO thereby decreasing exhaled levels.
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Lewis, A. "Modulation of the systemic inflammatory response syndrome in lower limb ischaemia-reperfusion injury". Thesis, Queen's University Belfast, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421004.
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Harkin, Denis William. "Modulation of the systemic inflammatory response syndrome in lower limb ischaemia-reperfusion injury". Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326388.
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Hoffman, Crystal Joyce. "Glucocorticoid Receptor Density and Binding Affinity in Horses with Systemic Inflammatory Response Syndrome". Thesis, Virginia Tech, 2014. http://hdl.handle.net/10919/48423.
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There were three objectives of this study. The first was to determine if commercially available fluorochromes could be used to determine the glucocorticoid receptor (GR) density and binding affinity (BA) in equine peripheral blood mononuclear cells. The second was to determine if there was a correlation between elevated plasma cortisol and GR density or binding affinity in healthy adult horses. The third objective was to evaluate the HPA axis in adult horses presenting with systemic inflammatory response syndrome (SIRS), and to determine where any alterations in HPA axis function occur in these patients compared to healthy adults. For the first part of the study, peripheral venous blood was collected from 3 healthy research horses on 3 days. Peripheral blood mononuclear cells were isolated using Ficoll gradient centrifugation. Phycoerythrin (PE)-CD44 was then used to extracellularly label leukocytes, and then an intracellular GR antibody was used to determine a baseline measurement of GR density and fluorescein isothiocyanate (FITC)-dexamethasone was used to determine binding affinity via flow cytometric analysis. Comparison of control samples to those for CD44, GR density, and GR binding affinity showed a statistically significant difference for all samples (P<0.0001, P<0.0001, and P<0.0001 respectively). This showed that the CD44, GR antibody, and FITC-dexamethasone could successfully be used to analyze equine peripheral blood mononuclear cells for GR activity.
For the second part of the study, an ACTH stimulation test was performed on 8 healthy horses in order to induce an increase in endogenous cortisol production. Plasma cortisol levels, GR density, and GR binding affinity were measured at baseline, 4, 8, and 24 hours after treatment. Median basal cortisol concentration was 4.9, range 3.2-6.1 μg/dl. This initially increased following ACTH stimulation to 5.6, range 4.8-7.4 μg/dl, then showed a significant decrease by 8 hours post ACTH administration to 1.4, range 1.1-2.7 μg/dl (P=0.0221). No correlation was observed between plasma cortisol concentration in healthy horses and GR density or binding affinity (r=-0.145, P=0.428 and r=0.046, P=0.802, respectively).
For the third phase of the study, horses (N=10) with systemic inflammatory response syndrome (SIRS) were compared to healthy, age and sex matched controls (N=10) presenting for lameness evaluation or ophthalmologic examination. Blood was collected from SIRS cases and controls on presentation to the Equine Medical Center. A CBC, serum biochemistry, and serum ACTH and cortisol measurements were performed. GR density and binding affinity were also determined. Nonsurvivors had a significantly decreased GR binding affinity (P=0.008) and demonstrated a trend towards an increase in the ACTH:cortisol ratio. ROC analysis was performed for serum ACTH and cortisol concentrations, the ACTH:cortisol ratio, GR density and GR binding affinity, and triglycerides to determine cut-off values associated with nonsurvival. These were then used to analyze this population using Fischer's exact test to determine the odds ratio (OR) associated with nonsurvival for each variable. This revealed that a serum triglyceride concentration greater than 28.5 mg/dl was associated with nonsurvival (OR=117, 95% CI, 1.94-7060). The other variables were not found to be significantly associated with nonsurvival, although a Delta BA% of less than 35.79% was found to be closely associated with nonsurvival (OR=30.33, 95% CI, 0.96-960.5). Additionally, a significant negative correlation was detected between the plasma ACTH concentration and Delta BA% (r=-0.685, P=0.029) and the ACTH:cortisol ratio and the Delta BA% (r=-0.697, P=0.025).
This study showed that nonsurviving horses with SIRS had a significantly decreased GR binding affinity compared to survivors, and a tendency toward an increase in their ACTH:cortisol ratios. This confirms that HPA axis dysfunction occurs in adult horses with SIRS as tissue resistance to glucocorticoids, and potentially relative adrenal insufficiency as well. These results suggest that there are horses with SIRS that might benefit from "physiologic" doses of synthetic glucocorticoids to complement their relative adrenal insufficiency in addition to their poor tissue sensitivity. Further research should focus on methods to more rapidly determine which horses might benefit from treatment with glucocorticoids on presentation, as well as to more accurately determine prognosis for survival.Master of Science
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Sutherland, Ainsley M. "Genetic determinants of the host response to infection in critically ill adults with systemic inflammatory response syndrome". Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/31527.
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Background. Activation of a systemic inflammatory response to infection varies significantly between individuals with important clinical implications. Genotype contributes substantially to outcome of infectious disease. Hypothesis. Allelic variants of inflammatory and innate immunity genes affect protein levels and function and are predictive of outcome in critically ill adults who have systemic inflammatory response syndrome (SIRS). Methods. Clinical data for derivation and validation cohorts of critically ill Caucasian patients with SIRS were collected for 28 days after admission to ICU and also for cardiac surgery patients. A subgroup of cardiac surgery patients had blood drawn post-operatively for cytokine measurements. Haplotypes of candidate genes were inferred from publicly available data using PHASE and cladistic structure determined using MEGA2. A set of "haplotype tag" single nucleotide polymorphisms (htSNPs) that defined major haplotype clades of the candidate genes and previously examined SNPs were chosen for genotyping in the three cohorts. Main results. CD14 -159TT was associated with Gram-negative cultures in the derivation cohort and with mortality in the validation cohort. Mannose-binding lectin (MBL) haplotype pairs XO/O and O/O were associated with positive bacterial cultures and TLR2 - 16933AA was associated with sepsis and with Gram-positive cultures in the derivation cohort. The C/T/A clade of IRAK4 was associated with Gram-positive cultures in a large derivation cohort and with decreased B-lymphocyte response to CpG and a trend to decreased fibroblast response to LPS. Haplotype clades of IL-6 were associated with 28-day mortality and organ dysfunction in the derivation cohort, but not in the validation cohort. Haplotype clades of IL-6 were associated with post-surgical vasodilation in cardiac surgery patients, but not with altered serum levels of cytokines after cardiac surgery. Conclusions. Variation in the key inflammatory and innate immunity genes IL-6, CD14, MBL and TLR2 contribute to variation in individuals' responses to inflammatory stimuli.Medicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate
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Pilypienė, Ingrida. "Significance of Foetal Inflammatory Response Syndrome on Health and Psychomotor Development in Premature Infants". Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2012. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2012~D_20120601_102857-39598.
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Improved perinatal care during the last few years has led to higher survival rates for preterm infants. However, with higher survival rates, the number of children demonstrating long-term health disorders that result in a poorer quality of life is increasing. The most common complications in those preterm children include motion disorders, vision and hearing impairment, mental disorders, and chronic lung disease. Intrauterine infection may cause foetal infection and inflammation thus inducing the inflammatory response in foetus, defined by foetal inflammatory response syndrome (FIRS). FIRS may cause a heavy damage in foetus and newborns as well as later disorders in the infant organism, such as cerebral palsy and chronic lung disease. Speaking about researches proving relation of the perinatal inflammatory response and psychomotor development in a preterm newborn, these are few. The foetal inflammatory response syndrome is a problem that has not been examined yet in Lithuania. Researches of cytokines in umbilical cord blood to make prognoses on the health and psychomotor development in a premature infant has not been performed either. Hopefully, the study results will allow a more detail explanation of the reasons for preterm delivery, better understanding of health disorders in premature infants and prognosis of the process of a child development. The aim of the study was to evaluate the importance of FIRS for the early and later adaptation of premature infants and for... [to full text]Dėl pagerėjusios perinatalinės priežiūros per pastaruosius metus neišnešiotų naujagimių išgyvenamumas labai pagerėjo. Tačiau, kai neišnešiotų naujagimių išgyvena vis daugiau, daugėja ir vaikų, kuriems augant, išryškėja ilgalaikiai sveikatos sutrikimai, pabloginantys jų gyvenimo kokybę. Nurodoma, kad dažniausia neišnešioto naujagimio gimimo priežastis yra intrauterinė infekcija, kuri progresuodama gali inicijuoti vaisiaus uždegiminio atsako sindromą, kurio metu vaisiuje suintensyvėja uždegiminių citokinų IL-1, IL-6, IL-8, TNF-α, augimo veiksnių gamyba. Šio sindromo pasekmė - sunkūs vaisiaus ir naujagimio pažeidimai bei vėlesni liekamieji kūdikio sveikatos sutrikimai, tokie kaip cerebrinis paralyžius ir lėtinė plaučių liga. Tyrimų, kurie rodytų perinatalinio uždegimo ir neišnešioto naujagimio psichomotorinės raidos sąsajas nėra daug. Ryšys tarp vaisiaus uždegimo ir neišnešiotų naujagimių retinopatijos atrastas neseniai, tad tyrimų šia kryptimi atlikta taip pat nedaug. Ryšys tarp perinatalinio uždegimo ir grėsmingų naujagimystės komplikacijų leidžia daryti prielaidą, kad neišnešioto naujagimio ankstyvas sveikatos vertinimas ir gyvenimo kokybės prognozė yra labai svarbūs, norint kuo anksčiau pradėti tikslinį gydymą bei ankstyvą vaiko raidos korekciją. Šio darbo tikslas buvo įvertinti vaisiaus uždegiminio atsako sindromo įtaką neišnešioto naujagimio sveikatai ir psichomotorinei raidai iki 1 metų koreguoto amžiaus. Tyrimo objektą sudarė virkštelės kraujo citokinų IL-6, bTNF-α... [toliau žr. visą tekstą]
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Davarya, Shekar Ligia. "Inflammatory and Thrombotic Responses to Microbial Products in Fetal Vessels Are Mediated through Divergent Toll-Like Receptor Signaling Pathways: Implications in Fetal Inflammatory Response Syndrome". Yale University, 2008. http://ymtdl.med.yale.edu/theses/available/etd-08072007-132134/.
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Placental vessels and the umbilical circulatory network function to carry oxygen and nutrients to the fetus. It is at this level that placental lesions such as villitis, obliterative vasculopathy, and thrombotic vasculopathy have been observed in association with fetal inflammatory response syndrome (FIRS) and cerebral palsy. We used human umbilical vein endothelial cells (HUVECs) as a model to study the regulation of inflammation and thrombosis in fetal vessels by microbial products. In this thesis we measured interleukin-8 (IL-8) and tissue factor (TF) expression by HUVECs treated with lipopolysaccharide (LPS), poly (I:C) (PIC), and peptidoglycan (PG). Our results show a profound induction of IL-8 by PIC, a TLR-3 ligand. We also show a moderate induction of tissue factor expression in PIC-treated HUVECs. These results show that HUVECs are exquisitely sensitive to PIC and suggests an important role for viral infection in umbilical vessel inflammation. We additionally treated HUVECs with dexamethasone (DEX), an anti-inflammatory steroid, and melatonin (MT), a pineal gland product with immunomodulatory and anti-oxidant properties. DEX reduced the level of both IL-8 and TF expression in PIC-treated cells. MT, however, further enhanced IL-8 expression in PIC-treated cells. Our results indicate a potential role for glucocorticoid therapy in reducing placental vessel inflammation and thrombosis. Thus, intervention with GC in pregnancies with FIRS may reduce the severity of placental lesions associated with cerebral palsy.
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Davarya, Shekar Ligia. "Inflammatory and thrombotic responses to microbial products in fetal vessels are mediated through divergent toll-like receptor signaling pathways implications in fetal inflammatory response syndrome /". [New Haven, Conn. : s.n.], 2007. http://ymtdl.med.yale.edu/theses/available/etd-08072007-132134/.
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Boyes, Simon Ashley. "The role of preoperative antioxidant status in the development of the systematic inflammatory response syndrome in elective aortic aneurysm repair". Thesis, University of Southampton, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.430709.
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Lahiri, Rajiv. "Changes in innate immune function predict post-operative systemic inflammatory response syndrome (SIRS) following major hepatico-pancreatico-biliary (HPB) surgery". Thesis, Queen Mary, University of London, 2014. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8952.
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Introduction Patients undergoing major surgery are at risk of life-threatening complications including systemic inflammatory response syndrome (SIRS) and sepsis. Early identification of patients at risk of SIRS would allow tailored post-operative care and improve survival. Elevated serum IL-6 levels have been shown patients with poor post-operative outcomes, but the mechanisms underlying this response are unknown. We studied these mechanisms in patients undergoing major surgery to identify early biomarkers of altered inflammatory responses and poor clinical outcomes. Methods Serial blood samples were taken from consenting, adult patients undergoing major hepatic or pancreatic surgery pre-operatively and on days one and two post-operatively. Patients with inflammatory co-morbidities, pre-operative sepsis and those taking anti-inflammatory medications were excluded. Peripheral blood mononuclear cells (PBMCs) were isolated, stimulated for 24 hours with lipopolysaccharide (LPS) or flagellin and cytokine production was quantified by ELISA. PBMC surface expression of CD14, CD16, TLR4 and TLR5 was assessed by flow cytometry. Transcription factor phosphorylation was evaluated using Phosflow. SIRS was defined by internationally agreed consensus criteria. Results Serum concentrations of IL-6 on postoperative Day 2 were significantly increased in 12 patients who developed SIRS (median postoperative day 6) compared with 27 patients who did not. PBMCs from SIRS patients following surgery (before clinical signs of SIRS) displayed significantly greater TLR4 and TLR5 expression and produced significantly more IL-6 in response to LPS and flagellin. Consistent with these data, TLR-driven phosphorylation of NF- 5 κB was increased post-operatively, and interferon alpha-mediated STAT1 phosphorylation was higher pre-operatively in SIRS patients. Differences in TLR4 and TLR5 expression were greatest in the CD14++CD16+ ‘intermediate’ monocyte population. Intermediate monocyte TLR4 and TLR5 expression post-operatively predicted SIRS development with an accuracy of 0.89 - 1.0 (calculated areas under the receiver operator curves). Conclusion Markers of innate immune dysfunction can be used 5 days before the onset of clinical signs to identify patients at risk of SIRS.
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Engel, Julia [Verfasser]. "Mittels Multiplate® Analyzer bestimmte Thrombozytenfunktion bei Kleinpferden und Ponys sowie bei Equiden mit Systemic Inflammatory Response Syndrome / Julia Engel". Gießen : Universitätsbibliothek, 2020. http://d-nb.info/1216143684/34.
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Schaefer, Helen Leanne [Verfasser]. "Investigations on the quantitative and qualitative protein excretion in urine of dogs with Severe Inflammatory Response Syndrome (SIRS) / Helen Leanne Schaefer". Berlin : Freie Universität Berlin, 2012. http://d-nb.info/1027151302/34.
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Gebhardt, Constance. "Systemic-inflammatory-response-Syndrome und Sepsis beim Hund : Untersuchung von klinischen, hämatologischen, blutchemischen und gerinnungsdiagnostischen Parametern sowie des C-reaktiven Proteins /". Berlin : Mbv, Mensch-und-Buch-Verl, 2009. http://d-nb.info/998071498/04.
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Cavalcante, Ana Augusta Monteiro. "Enteral nutrition supplemented with l-glutamine and its action on the inflammatory process, the glycolytic metabolism, the immune system and the oxidative stress of patients with systemic inflammatory response syndrome". Universidade Federal do CearÃ, 2010. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=5260.
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Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgicoThe Systemic Inflammatory Response Syndrome (SIRS) is characterized by an excessive release of inflammatory mediators as a systemic inflammatory response to a serious clinical injuries. The use of glutamine in nutraceutical doses has been studied as a strategy in tissue protection and preservative of tissue metabolic function in stressful situations, helping to improve the immune response of patients. The effects of enteral glutamine supplementation in nutraceutical doses on the inflammatory markers, of glycolytic metabolism, of immune system and of oxidative stress were studied in adult and elderly patients with SIRS in a prospective, clinical, randomized, controlled, double-blind crossover study. Thirty six moderately severe patients admitted to the Intensive Care Unit were selected according to pre-defined criteria, diagnosis of SIRS and the APACHE II score (>10<20), distributed into two groups and submitted to the supplementation with 1 litre of enteral nutrition with addition of 30g of L-glutamine or calcium caseinate or 1 litre of enteral nutrition with addition of 30g of calcium caseinate or L-glutamine for two days, pause for one day only with diet, followed by four days of supplementation. Blood samples were collected before (T0) and after (T1) each supplementation. For evaluation blood parameters (hematocrit, leukocytes, lymphocytes, monocytes, prealbumin, blood urea nitrogen, creatinine, glucose, lactate, C-peptide and insulin), IL-1, IL-6, IL-10 and TNFα were also assayed. Glutathione, TBARS, and glutamine and glutamate amino acids were measured. Six patients died during the study. Thirty patients finished the study, 16 men (53%) and 14 (47%) women, median age 74.4 years (30-92 years) in moderately severe state of health (APACHE II 13.1 - range 10-19). All patients developed SIRS and were given enteral nutrition supplemented with L-glutamine or calcium caseinate, 1464kcal/day (range 792-1914kcal/day). The use of L-glutamine in nutraceutical dose of 30g/day showed no changes in blood parameters. All laboratory parameters remained within normal values except the blood urea [Calcium Caseinate T1=47.0mg/dL (range 34.0-69.0 mg/dL) versus Glutamine T1=50.0mg/dL (36.75-75.0mg/dL); p=0.030]. Creatinine concentrations were not statistically different. There was no statistically significant difference in assessment of inflammatory parameters (IL-1, IL-6, IL-10 E TNFα). Leukocytes count decreased significantly in both groups [Calcium Caseinate T0=13.650 1/mm3 (10.148-18.250 1/mm3) versus T1=11.500 1/mm3 (8.050-29.100 1/mm3); p=0,019] and [Glutamine T0=12.850 1/mm3 (11.155-15.550 1/mm3) versus T1=11.000 1/mm3 (9.200-16.325 1/mm3); p=0.046]. There was increase statistically significant difference in lymphocytes count between groups [Calcium Caseinate T1=1085 1/mm3 (range 805-1363 1/mm3) versus Glutamine T1=1916 1/mm3 (1301-2517 l/mm3); p<0.0001] and Calcium Caseinate group decreases [T0=1288 1/mm3 (range 834-2209 1/mm3) versus T1=1085 1/mm3 (range 805-1363 1/mm3); p=0.0324] and Glutamine group increases [T0=954 1/mm3 (range 785-1442 1/mm3) versus T1=1916 1/mm3 (range 1301-2517 l/mm3); p<0.0001]. Blood concentration of TBARS decreased significantly in both groups [Calcium Caseinate T0=20.56mol MDA/ml (range 13.64-20.56mol MDA/ml); p=0.001] and [Glutamine T0=17.67 mol MDA/ml (range 8.11-34.98 mol MDA/ml) versus T1=16.52 mol MDA/ml (range 5.41-21.86 mol MDA/ml); p=0.020]. The blood concentrations of Gluthatione showed a statistically significant reduction in caseinate group (T0=486.0mol/ml (range 486.0Â165.8mol/ml versus T1=451.0Â167.4mol/ml; p=0.047) and no statistically significant difference in the glutamine group, nor between groups. However, there were no differences between groups. Glutamine and glutamate were not statistically different. Enteral nutrition supplemented with glutamine in nutraceutical doses of 30g/day increase lymphocyte count, helps to reduce lipid peroxidation and maintains the antioxidant glutathione capacity, interfering beneficially modulating the inflammatory response and stress, but present no effect upon cytokines concentrations or glycolytic parameters.
A SÃndrome da Resposta InflamatÃria SistÃmica (SRIS) caracteriza-se por uma liberaÃÃo excessiva de mediadores inflamatÃrios a uma sÃrie de situaÃÃes clÃnicas graves. A utilizaÃÃo da glutamina em doses nutracÃuticas tem sido estudada como uma estratÃgia de proteÃÃo tecidual e metabÃlica em situaÃÃes de estresse, melhorando a resposta imune de pacientes. Os efeitos da nutriÃÃo enteral suplementada com 30g/dia de glutamina sobre os marcadores inflamatÃrios, do metabolismo glicolÃtico, da funÃÃo imune e do estresse oxidativo foram estudados em pacientes adultos e idosos com SRIS. Foi realizado estudo clÃnico prospectivo, randomizado, controlado, duplo-cego, cruzado. Trinta e seis pacientes internados em Unidade de Terapia Intensiva foram selecionados pelos critÃrios do estudo, diagnÃstico da SRIS e score APACHE II (>10<20), distribuÃdos em dois grupos e submetidos à suplementaÃÃo com 1 litro de dieta enteral suplementada com 30g de L-glutamina ou caseinato de cÃlcio ou 1 litro de dieta enteral suplementada com 30g de caseinato de cÃlcio ou L-glutamina por dois dias, intervalo de um dia somente com dieta, perfazendo quatro dias de dieta com suplementaÃÃo. Amostras de sangue foram coletadas antes (T0) e apÃs (T1) cada suplementaÃÃo. Foram realizadas anÃlises do hematÃcrito, leucÃcitos, linfÃcitos, monÃcitos, prÃ-albumina, urÃia, creatinina, glicose, lactato, peptÃdeo-C e insulina, das IL-1, IL-6, IL-10, TNFα, glutationa, TBARS e dos aminoÃcidos glutamina e glutamato. Seis pacientes foram a Ãbito durante o estudo e trinta pacientes concluÃram o estudo, sendo 16(53%) homens e 14(47%) mulheres, mediana de idade 74,4 anos (30-92 anos), moderadamente graves, mediana de APACHE II 13,1 (10-19) e mediana de ingestÃo calÃrica de 1464kcal/dia (792-1914kcal/dia). O uso L-glutamina em dose nutracÃutica de 30g/dia nÃo mostrou alteraÃÃes nos parÃmetros hematolÃgicos. Houve aumento da urÃia [Caseinato T1=47,000mg/dL (34,000-69,000mg/dL) versus Glutamina T1=50,000mg/dL (36,750-75,000mg/dL); p=0,030] na comparaÃÃo intergrupos, mas nÃo houve diferenÃa estatisticamente significante de creatinina em nenhum dos grupos. NÃo houve alteraÃÃo estatisticamente significante nos parÃmetros inflamatÃrios (IL-1, IL-6, IL-10 e TNFα). A contagem de leucÃcitos diminuiu significantemente em ambos os grupos [Caseinato T0=13.650 1/mm3 (10.148-18.250 1/mm3) versus T1=11.500 1/mm3 (8.050-29.100 1/mm3); p=0,019] e [Glutamina T0=12.850 1/mm3 (11.155-15.550 1/mm3) versus T1=11.000 1/mm3 (9.200-16.325 1/mm3); p=0,046]. Houve aumento estatisticamente significante na contagem de linfÃcitos na comparaÃÃo intergrupos [Caseinato T1=1.085 1/mm3 (805-1.363 1/mm3) versus Glutamina T1=1.916 1/mm3 (1.301-2.517 l/mm3); p<0,0001], uma diminuiÃÃo estatisticamente significante no grupo Caseinato [T0=1.288 1/mm3 (834-2.209 1/mm3) versus T1=1.085 1/mm3 (805-1.363 1/mm3); p=0,0324] e aumento no grupo Glutamina [T0=954 1/mm3 (785-1.442 1/mm3) versus T1=1.916 1/mm3 (1.301-2.517 l/mm3); p<0,0001]. Observou-se reduÃÃo estatisticamente significante na dosagem do TBARS na comparaÃÃo intragrupos [Caseinato T0=20,56mol MDA/ml (13,64-20,56mol MDA/ml) versus T1=15,08 mol MDA/ml (13,64-20,56 mol MDA/ml); p=0,001] e [Glutamina T0=17,67 mol MDA/ml (8,11-34,98 mol MDA/ml) versus T1=16,52 mol MDA/ml (5,41-21,86 mol MDA/ml); p=0,020], mas nÃo houve diferenÃas intergrupos. A concentraÃÃo sanguÃnea de glutationa apresentou uma reduÃÃo estatisticamente significante no grupo Caseinato (T0=486,00mol/mlÂ165,80mol/ml) versus T1=451,00Â167,40mol/ml; p=0,047) e nÃo houve diferenÃa no grupo Glutamina, tampouco entre os grupos. Glutamina e glutamato nÃo demonstraram diferenÃas estatisticamente significantes. Conclui-se que a nutriÃÃo enteral suplementada com glutamina em dose nutracÃutica de 30g/dia em pacientes moderadamente graves promove um aumento dos linfÃcitos, contribui para reduzir a peroxidaÃÃo lipÃdica e mantÃm a capacidade antioxidante da glutationa, interferindo de forma benÃfica na modulaÃÃo da resposta inflamatÃria e do estresse, mas nÃo apresenta nenhum efeito sobre a concentraÃÃo de citocinas ou parÃmetros glicolÃticos.
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Machaca, Quea Nancy Roxana, Ventura Sonia Salazar e Teves Pedro Montes. "Síndrome de respuesta inflamatoria sistémica como indicador pronóstico en pacientes cirróticos hospitalizados". Sociedad de Gastroenterología del Perú, 2014. http://hdl.handle.net/10757/331955.
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narmq2@hotmail.comObjetivo: La inflamación sistémica empeora los trastornos circulatorios en el paciente cirrótico y recientemente el síndrome de respuesta inflamatoria sistémica (SRIS) podría ser un indicador pronóstico en ellos. El objetivo del estudio fue determinar si la presencia de SRIS al ingreso en pacientes cirróticos hospitalizados está asociada a complicaciones o mortalidad. Materiales y métodos: Estudio de cohortes retrospectiva, realizado en el Hospital Nacional Daniel Alcides Carrión. Se admitieron pacientes cirróticos hospitalizados desde julio 2008 hasta diciembre 2010 sin comorbilidades importantes, neoplasia maligna, infección VIH, o estancia fue menor a 72 horas. Se evaluó presencia de SRIS al ingreso y la aparición de complicaciones o muerte después de 72 horas del ingreso. Resultados: Fueron 150 pacientes cirróticos admitidos, se excluyeron 6, tres por supervivencia menor a las 72 horas, uno por neoplasia, uno por insuficiencia cardiaca severa y dos por insuficiencia renal crónica. En total 144 pacientes ingresaron al estudio, 95 (66%) pacientes presentaron SRIS al ingreso. No hubo diferencia significativa en cuanto a edad, sexo, etiología, en ambos grupos. SRIS estuvo asociado a mayores puntajes de MELD y Child-Pugh Turcotte. De los pacientes con SRIS, 41 (43%) se complicaron y 16 (16,8%) fallecieron, mientras que del grupo sin SRIS 5 (10,2%) se complicaron y 2 (4%) fallecieron , ( p <0,0001y p =0,028 respectivamente). Las complicaciones más frecuentes fueron las infecciones y encefalopatía hepática. En el análisis multivariado SRIS estuvo asociado a complicaciones ( p <0,006) mas no a mortalidad ( p <0,276). Conclusiones: SRIS es frecuente en pacientes cirróticos hospitalizados y está asociado a complicaciones intrahospitalarias.
Objective: The systemic inflammation worsens circulatory disorders in cirrhotic patients and recently the systemic inflammatory response syndrome (SIRS) may be a prognostic indicator therein. The aim of the study was to determine whether the presence of SIRS at admission in hospitalized cirrhotic patients is associated with complications or mortality. Materials and methods: A retrospective cohorts study was conducted at the Daniel Alcides Carrion National Hospital. Hospitalized cirrhotic patients admitted from July 2008 to December 2010 without significant comorbidities, malignancy, HIV infection, or stay less than 72 hours were included. Presence of SIRS at admission and the occurrence of complications or death after 72 hours of admission were evaluated. Results: 150 cirrhotic patients were admitted, six were excluded; three for lower survival at 72 hours, one for neoplasia, one for severe heart failure and two for chronic renal failure. One hundred forty four patients were included, 95 (66%) patients had SIRS at admission. There was no significant difference in age, sex, etiology, in both groups. SIRS was associated with higher scores of MELD and Child-Turcotte Pugh. Of the group of patients with SIRS, 41 (43%) had complications and 16 (16.8%) died, while the group without SIRS 5 (10.2%) had complications and two (4%) died ( p <0.0001 and p =0.028 respectively). The most common complications were infections and hepatic encephalopathy. In multivariate analysis SIRS was associated with complications ( p <0.006) but not with mortality ( p <0.276). Conclusions: SIRS is common in hospitalized cirrhotic patients and is associated with in-hospital complications.
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Ortlieb, Lutz Volker [Verfasser]. "Bedeutung eines Fast-Track-Konzeptes für die systemische Inflammation (systemic inflammatory response syndrome = SIRS) nach offener Aneurysmaausschaltung [[Elektronische Ressource]] / Lutz Volker Ortlieb". Ulm : Universität Ulm. Medizinische Fakultät, 2013. http://d-nb.info/1036215199/34.
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Gebhardt, Constance [Verfasser]. "Systemic Inflammatory Response Syndrome und Sepsis beim Hund : Untersuchung von klinischen, hämatologischen, blutchemischen und gerinnungsdiagnostischen Parametern sowie des C-reaktiven Proteins / Constance Gebhardt". Berlin : Freie Universität Berlin, 2009. http://d-nb.info/1023751461/34.
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Pilypienė, Ingrida. "Vaisiaus uždegiminio atsako sindromo įtaka neišnešioto naujagimio sveikatai ir psichomotorinei raidai". Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2012. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2012~D_20120601_102908-05709.
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Dėl pagerėjusios perinatalinės priežiūros per pastaruosius metus neišnešiotų naujagimių išgyvenamumas labai pagerėjo. Tačiau, kai neišnešiotų naujagimių išgyvena vis daugiau, daugėja ir vaikų, kuriems augant, išryškėja ilgalaikiai sveikatos sutrikimai, pabloginantys jų gyvenimo kokybę. Nurodoma, kad dažniausia neišnešioto naujagimio gimimo priežastis yra intrauterinė infekcija, kuri progresuodama gali inicijuoti vaisiaus uždegiminio atsako sindromą, kurio metu vaisiuje suintensyvėja uždegiminių citokinų IL-1, IL-6, IL-8, TNF-α, augimo veiksnių gamyba. Šio sindromo pasekmė - sunkūs vaisiaus ir naujagimio pažeidimai bei vėlesni liekamieji kūdikio sveikatos sutrikimai, tokie kaip cerebrinis paralyžius ir lėtinė plaučių liga. Tyrimų, kurie rodytų perinatalinio uždegimo ir neišnešioto naujagimio psichomotorinės raidos sąsajas nėra daug. Ryšys tarp vaisiaus uždegimo ir neišnešiotų naujagimių retinopatijos atrastas neseniai, tad tyrimų šia kryptimi atlikta taip pat nedaug. Ryšys tarp perinatalinio uždegimo ir grėsmingų naujagimystės komplikacijų leidžia daryti prielaidą, kad neišnešioto naujagimio ankstyvas sveikatos vertinimas ir gyvenimo kokybės prognozė yra labai svarbūs, norint kuo anksčiau pradėti tikslinį gydymą bei ankstyvą vaiko raidos korekciją. Šio darbo tikslas buvo įvertinti vaisiaus uždegiminio atsako sindromo įtaką neišnešioto naujagimio sveikatai ir psichomotorinei raidai iki 1 metų koreguoto amžiaus. Tyrimo objektą sudarė virkštelės kraujo citokinų IL-6, bTNF-α... [toliau žr. visą tekstą]Improved perinatal care during the last few years has led to higher survival rates for preterm infants. However, with higher survival rates, the number of children demonstrating long-term health disorders that result in a poorer quality of life is increasing. The most common complications in those preterm children include motion disorders, vision and hearing impairment, mental disorders, and chronic lung disease. Intrauterine infection may cause foetal infection and inflammation thus inducing the inflammatory response in foetus, defined by foetal inflammatory response syndrome (FIRS). FIRS may cause a heavy damage in foetus and newborns as well as later disorders in the infant organism, such as cerebral palsy and chronic lung disease. Speaking about researches proving relation of the perinatal inflammatory response and psychomotor development in a preterm newborn, these are few. The foetal inflammatory response syndrome is a problem that has not been examined yet in Lithuania. Researches of cytokines in umbilical cord blood to make prognoses on the health and psychomotor development in a premature infant has not been performed either. Hopefully, the study results will allow a more detail explanation of the reasons for preterm delivery, better understanding of health disorders in premature infants and prognosis of the process of a child development. The aim of the study was to evaluate the importance of FIRS for the early and later adaptation of premature infants and for... [to full text]
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Corrêa, Sílvia Verônica de Magalhães e. "Avaliação da tromboelastografia em cães clinicamente normais e na detecção precoce da coagulação intravascular disseminada (CID) em cães com pancreatite". Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/10/10136/tde-08052017-100403/.
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A Coagulação Intravascular Disseminada (CID) é uma síndrome caracterizada pela ativação sistêmica da coagulação sanguínea, levando à trombose microvascular difusa e podendo comprometer a função de múltiplos órgãos. O acelerado consumo de plaquetas e fatores de coagulação pode, no entanto, dar origem a um estado de hipocoagulabilidade, o que confere à CID uma característica paradoxal na qual o excesso de coagulação pode causar uma diátese hemorrágica. Doenças que levam à Síndrome de Resposta Inflamatória Sistêmica (SIRS) estão entre os principais gatilhos da CID. A pancreatite é uma dessas doenças. O maior desafio para o médico veterinário é diagnosticar a CID na fase precoce, silenciosa e de hipercoagulabilidade, visto que os testes laboratoriais de rotina, como contagem de plaquetas, tempo de protrombina (TP) e tempo de tromboplastina parcial ativada (TTPA), detectam apenas o estado de hipocoaguabilidade, que se estabelece na fase mais avançada da síndrome. Nesse contexto ganham importância os analisadores tromboelastográficos, equipamentos que avaliam a coagulação em sangue total e que, ao menos em tese, podem informar a velocidade de formação do coágulo, a força máxima que ele atinge e os padrões de sua dissolução. Este estudo é o primeiro realizado em cães com o aparelho ReoRox G2 (MediRox), uma da marcas disponíveis no mercado. Limites de referência para as variáveis do aparelho foram definidos a partir da análise do sangue de 49 animais clinicamente saudáveis para três tipos de reação: acelerada com fator tecidual (TF), acelerada com TF e um antagonista de agregação plaquetária (abciximab) e apenas com sangue recalcificado. Em seguida, foram comparados a esse intervalo de referência os valores obtidos pela análise tromboelastográfica do sangue de seis pacientes com pancreatite recém-diagnosticada. Nos três tipos de reação pelo menos 50% dos pacientes do Grupo Pancreatite apresentaram alterações sugestivas de hipercoagulabilidade. A variável MAXELAST (força máxima do coágulo) foi a que esteve alterada com mais frequência entre os animais doentes. Não houve alteração nos marcadores de velocidade de fibrinólise. Estudos prospectivos que associem outras variáveis de trombose, protocolos de tratamento e prognóstico de pacientes com doenças subjacentes que predisponham à CID são necessários para que se possa afirmar que o traçado obtido pela tromboelastografia realmente representa um estado de hipercoagulabilidade in vivo em pacientes com pancreatite.Disseminated Intravascular Coagulation (DIC) is a syndrome characterized by systemic activation of blood clotting, leading to diffuse microvascular thrombosis and may compromise multiple organ function. The accelerated consumption of platelets and coagulation factors may, however, originate a state of hypocoagulability, which gives the DIC a paradoxical characteristic in which excess coagulation can lead to a hemorrhagic diathesis. Diseases which cause Systemic Inflammatory Response Syndrome (SIRS) are among the major triggers of DIC, including pancreatitis. The greatest challenge for veterinarians is to diagnose DIC in the early, silent and hypercoagulable phase, since routine laboratory tests, such as platelet count, prothrombin time (PT) and activated partial thromboplastin time (APTT), detect only the state of hypocoagulability, which occurs in the most advanced stage of the syndrome. In this context, thromboelastography analyzers stand out. They are equipment which evaluate coagulation in whole blood and, at least in theory, inform the speed of clot formation, its maximum force and how it dissolves. This is the first study performed in dogs with the ReoRox G2 (MediRox), one of the brands available in the market. Limits of reference were defined from blood analysis of 49 healthy animals for three reaction types: accelerated with tissue factor (TF), accelerated with TF and a platelet aggregation antagonist (abciximab) and with only recalcified blood. Next, values obtained by blood thromboelastographic analysis of six patients with newly diagnosed pancreatitis were compared to this reference range. In all three types of reactions, at least 50% of patients in the Pancreatitis Group presented alterations suggestive of hypercoagulability. The variable MAXELAST (maximum clot strength) was the one that was most frequently altered among ill animals. There was no change in fibrinolysis rate markers. Prospective studies associating other thrombosis variables, treatment protocols, and prognosis of patients with underlying diseases predisposing to DIC are necessary to confirm that the pathway obtained by thromboelastography actually represents a state of hypercoaguability in vivo in patients with pancreatitis.
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Geerken, Luer Christian [Verfasser], e Frank [Akademischer Betreuer] Hildebrand. "Effekte des Interleukin-6 im Rahmen des Systemic Inflammatory Response Syndrome (SIRS) beim Polytrauma an einem Interleukin-6-knock-out-Modell der Maus / Luer Christian Geerken. Unfallchirurgische Klinik der Medizinischen Hochschule Hannover. Betreuer: Frank Hildebrand". Hannover : Bibliothek der Medizinischen Hochschule Hannover, 2011. http://d-nb.info/1017732655/34.
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Luo, Karen Yao. "Assessment of the Effect of Induced Hypothermia in Experimental Sepsis Using a Cecal Ligation and Perforation Mouse Model". Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20119.
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Sepsis-induced organ failure is associated with high morbidity and mortality
rates. The onset of an exaggerated host response to microbial invasion and/or trauma, is believed to be the primary cause of excessive inflammation and the subsequent tissue hypoperfusion observed in patients with severe sepsis. In our mouse model of sepsis induced by cecal ligation and perforation (CLP), symptoms indicative of the disease, including diarrhea, increased ventilation and persistent hypothermia, are present at six hours after the surgery (T6). In the untreated CLP mice, mortality occurs starting at T15. As induced hypothermia has shown to exert immunomodulatory effects, this study is aimed at assessing its potential in attenuating inflammation and improving survival in experimental sepsis. Our data has shown that deep hypothermia initiated at T6, by means of cold chamber-induced cooling, prolongs survival. Plasma cytokine quantification by enzyme-linked immunosorbent assays (ELISA) also reveals that induced deep hypothermia reduces tumour necrosis factor(TNF)-α and interleukin (IL)-6 production in untreated CLP mice. In contrast, induced moderate hypothermia does not have such effect. Antibiotic (cefotaxime) and saline resuscitation initiated immediately following CLP ensures survival. However, when these supportive treatments are initiated at T6, >50% mortality is observed in the CLP mice with or without induced hypothermia. In summary, this preliminary study provides proof for a downregulated inflammatory response mediated by external cooling. However, to achieve a survival benefit, treatment strategies in addition to cooling and antibiotics may be required.
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Alves, Maxley Martins. "INFLUÊNCIA DO SORO LÁTEX NATURAL DA SERINGUEIRA Hevea Brasiliensis SOBRE A RESPOSTA INFLAMATÓRIA AGUDA INDUZIDA POR SEPSE: ESTUDO EXPERIMENTAL EM RATOS". Pontifícia Universidade Católica de Goiás, 2014. http://localhost:8080/tede/handle/tede/2985.
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Previous issue date: 2014-09-03The acute inflammatory answer is a manifestation of the organism triggered by an infectious or non-infectious taunting. Predisposal factors are, for instance: bacteria, viruses, amongst other microorganisms or traumas. It is an internal survival mechanism. The development of a cascade of immunological events in an attempt of destroying an aggressive agent, with cardiologic, hemodynamic, respiratory, renal, endocrine, metabolic, gastrointestinal and hematological alterations occurs determining a syndrome clinic case. Vascular and immunological alterations trigger a counter balance inflammatory response. Recent researches using a specific derived fraction of the natural gum of Hevea brasiliensis rubber tree, called Hev b 13, has shown induction capability to synthesize interleukin 10 (IL-10) in vitro, stimulating the anti-inflammatory response that may result in homeostasis. These evidences are assessed with high mortality sepis induction, after surgical procedure with gastric, intestinal and pancreatic damaging and strain infusion of Acinetobacter baumanni of resistance profile to multiple antibiotics tested. In dose 0,5 mg/kg of Hev b 13 solution, subcutaneous, similarities were observed in the survival of animals treated with this solution and the control group, treated with 1 ml of SF0, 9% (p= 0,8106). The laboratorial analysis, on the other hand, showed total leukocytes reckoning (p = 0,0207) and total lymphocyte (p= 0,0032) with statistically significant differences. In further counting there was no significant difference (p>0,05). The Hev b 13 solution may lead to the induction of reducing the amplification of immunological cellular cascade, reducing the production of total leukocytes and lymphocytes, with effect over the immunological response, anti-inflammatory effect. The experiment induced synthesis of interleukin-10 (IL-10) and tumor necrosis factor (TNF). Rats receiving Hev b 13, lung tissue showed lesser involvement of inflammatory cells.
A resposta inflamatória aguda é uma manifestação do organismo desencadeada por um insulto. Fatores que predispõem são, por exemplo: bactérias, vírus, dentre outros micro-organismos ou traumas. É um mecanismo interno de sobrevivência. A resposta inflamatória leva ao desenvolvimento de uma cascata de eventos imunológicos na tentativa de destruir o agente agressor, com alterações cardiológicas, hemodinâmicas, respiratórias, renais, endocrinometabólicas, gastrointestinais e hematológicas determinando um quadro clínico sindrômico. As alterações vasculares e imunológicas desencadeiam uma resposta de contra-balanço inflamatória. Pesquisas recentes utilizando uma fração específica derivada do látex natural da seringueira Hevea brasiliensis, denominada Hev b 13, tem mostrado capacidade de induzir síntese de interleucina 10 (IL-10) in vitro, estimulando a resposta anti-inflamatória, podendo resultar em homeostase. Estas evidências são avaliadas no modelo experimental adotado com indução de sepse grave, após procedimento cirúrgico com lesões gástrica, intestinal e pancreática, além de infusão de cepas de Acinetobacter baumanni com perfil de resistência a múltiplos antibióticos testados. Foi infundido solução Hev b 13 via subcutânea na dosagem 0,5 mg/Kg. Observou-se semelhança na sobrevida dos animais que foram tratados com esta solução e os animais do grupo controle, tratados com 1 ml de SF0,9% (p =0 ,8106). A contagem de leucócitos totais (p= 0,0207) e linfócitos totais (p= 0,0032) apresentou diferenças estatisticamente significativas. Nas demais células as contagens não apresentaram diferença estatística significativa (p>0,05). A solução de Hev b 13 pode induzir a redução da amplificação da cascata celular imunológica, reduzindo a produção de leucócitos e linfócitos totais, modulando a resposta imunológica. O experimento realizado induziu síntese de interleucina 10 (IL-10) e Fator de necrose tumoral (TNF). Os ratos que receberam Hev b 13, apresentaram no tecido pulmonar menor envolvimento de células inflamatórias.
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Mercke, William L. "Diagnosis of Systemic Inflammation Using Transendothelial Electrical Resistance and Low-Temperature Co-fired Ceramic Materials". UKnowledge, 2013. http://uknowledge.uky.edu/cme_etds/21.
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Systemic inflammation involves a complex array of cytokines that can result in organ dysfunction. Mortality remains high despite the vast amount of research conducted to find an effective biomarker. The cause of systemic inflammation can be broad and non-specific; therefore, this research investigates using transendothelial electrical resistance (TEER) measurements to better define systemic inflammatory response syndrome (SIRS)/sepsis within a patient. Results show a difference in TEER measurements between healthy individuals and SIRS-rated patients. This research also displays correlations between TEER measurements and biomarkers currently studied with systemic inflammation (tumor necrosis factor-α, C- reactive protein, procalcitonin). Furthermore, this research also presents the groundwork for developing a microfluidic cell-based biosensor using low temperature co-fired ceramic materials. An LTCC TEER-based microfluidic device has the potential to aid in a more effective treatment strategy for patients and potentially save lives.
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Sauer, Carlos Roberto de Oliveira 1968. "Avaliação da prevalência da síndrome da resposta inflamatória sistêmica no pós-operatório da cirurgia estética de mama : uma contribuição para os cuidados perioperatórios". [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309374.
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Orientador: Francisco Hideo AokiDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: Introdução: Síndrome da resposta inflamatória sistêmica (SRIS) é uma situação clínica na qual ocorrem as alterações fisiológicas da sepse, mas que é desencadeada por uma agressão não infecciosa ao organismo. Foi definida em 1991, em consenso internacional, e, assim como a sepse, está associada à insuficiência de múltiplos órgãos e sistemas (IMOS) e à mortalidade. Não há muitos dados epidemiológicos a respeito da SRIS, mas sabe-se que a sepse grave e choque séptico são juntos a principal causa de morte nas unidades de terapia intensiva (UTIs) não coronarianas nos EUA e,no Brasil, são responsáveis por mais de 54.000 internações anualmente, com uma mortalidade associada de 32,9% e 64,1%, para sepse grave e choque séptico, respectivamente. Após documentar, em estudo fisiológico com cateter de artéria pulmonar, um caso de choque distributivo com depressão do miocárdio no pós-operatório imediato de uma cirurgia redutora de mama, sem qualquer associação a quadro infeccioso, foi feita, sem sucesso, uma extensa busca de casos semelhantes na literatura médica. Inclusive, nesta revisão, foi encontrada uma grande incidência de cirurgias estéticas de mama no Brasil: quase 280.000 por ano, dentre as quais 131.000 são mamoplastias redutoras. Objetivos: avaliar a prevalência de SRIS e SRIS grave no pós-operatório da cirurgia estética de mama e, secundariamente, avaliar os fatores de risco associados a sua ocorrência e discutir as possíveis implicações da SRIS nos cuidados peri-operatórios das cirurgias estéticas de mama. Casuística e método: foram realizados dois estudos epidemiológicos, um retrospectivo no Hospital Estadual de Sumaré¿UNICAMP (HES), a mesma instituição onde foi verificado esse caso de SRIS grave, envolvendo todas as pacientes que foram submetidas somente a mamoplastia redutora (de 2001 a 2012, com 154 pacientes) e outro estudo prospectivo no Hospital do Instituto do Coração de Campinas (Hospital ICC), onde também foram avaliadas pacientes submetidas à inserção e à troca de próteses mamárias, associadas ou não à lipoaspiração (primeiro semestre de 2012, com 24 pacientes). Resultados: no HES encontrou-se 17 casos de SRIS (11,0%) e três casos de SRIS grave (1,9%), sendo verificado, dentre estes, um caso de SRIS grave com choque. Não houve diferença entre os grupos de pacientes com e sem SRIS para 29 variáveis clínicas,-epidemiológicas e farmacológicas analisadas. Observou-se uma tendência a maior frequência de SRIS em pacientes submetidas a anestesia por halogenados, mas sem significância estatística (p>0,05). No estudo do Hospital ICC foi verificada uma prevalência de SRIS 29,2%. Nesse segundo estudo, além de se aproximar da realidade das cirurgias estéticas de nosso país, pois foi feito em um hospital particular não ligado a qualquer universidade, pudemos contar com o critério do leucograma, colhido após a cirurgia. Após exaustiva revisão da literatura médica, foram encontrados alguns possíveis fatores confundidores da análise, a saber:os anestésicos inalatórios (halogenados e óxido nitroso), o propofol, a anestesia peridural, o próprio tecido mamário (em sua anatomia e fisiologia apresenta interfaces com sistema imune) e o órgão adiposo (participa da constituição da mama e possui funções endócrinas, além de ser ontologicamente ligado ao sistema imune). Ao revisar o tipo de cirurgia realizado e a fisiopatogenia da SRIS, encontramos mais duas questões com relevância em termos saúde coletiva: a imunossupressão e a ativação da cascata de coagulação associadas à SRIS poderiam gerar uma população de mulheres mais suscetíveis às complicações infecciosas, à trombose venosa profunda (TVP) e ao trombo-embolismo pulmonar (TEP). Novamente, foram feitos novos levantamentos bibliográficos para abordar estas questões, sendo encontradas inúmeras referências associando o uso inadequado de antibióticos a complicações bacterianas (superinfecções) e artigos descrevendo, nesta situação específica de pós-operatório, o frequente descumprimento dos protocolos de profilaxia de TVP/TEP. Conclusão: na cirurgia estética de mama ocorre uma incidência de SRIS próximo a 30% (quando são utilizados os 4 critérios diagnósticos de SRIS) e uma incidência de SRIS grave de quase 2%. Também foi descrito um caso clínico de SRIS grave com choque no pós-operatório da cirurgia estética de mama, algo presente no dia a dia dos profissionais que atendem estas pacientes, mas sem prévio relato na literatura médica. Não foi encontrada qualquer associação entre SRIS e os fatores de risco analisados. É necessário estarmos atentos para uma melhor definição da importância deste quadro em termos de saúde pública, com um olhar protetor para a população de mulheres submetidas à cirurgia estética de mama, vulneráveis às complicações do pós-operatório numa frequência que pode ser maior que a esperada
Abstract: Introduction : SIRS is a clinical situation where the physiological changes due to sepsis occur, but triggered by a noninfectious aggression to the organism. It was defined in 1991, with international consensus, and like sepsis it is associated to multiple system organ failure (MSOF) and mortality. There is not much epidemiological data related to SIRS but it is known that severe sepsis and septic shock are together the leading cause of death in non-coronary ICUs in the U.S. and, In Brazil, they are responsible for more than 54,000 hospitalizations annually, with an associated mortality of 32.9% and 64.1% for severe sepsis and septic shock, respectively. After reporting, in a physiological study of pulmonary artery catheter, a case of septic shock with myocardial depression in the immediate postoperative of reductive mammoplasty, without any sign of infection, an extensive literature review was done without success, seeking similar cases in the medical literature. Moreover, in this review, a high frequency of cosmetic surgery in breast were found in Brazil: almost 280,000 per year, of which 131,000 were reductive mammoplasties. Objective: Assess the prevalence of SIRS and severe SIRS in the postoperative of cosmetic breast surgery and , secondarily , assess the risk factors associated to its occurrence and discuss the possible implications of SIRS in the perioperative care of cosmetic breast surgery. Patients and Methods: Two epidemiological studies were conducted, one was a retrospective epidemiological survey which took place at the Sumaré State Hospital ¿ UNICAMP, the same institution where this case was found, involving all patients who underwent reduction mammoplasty ( from 2001 to 2012, with 154 patients) and the other was a prospective study developed at the Campinas Heart Institute Hospital, where patients subjected to placement and replacement of breast implants, associated or not to liposuction were assessed (first semester of 2012, with 24 patients). Results At the Sumaré State Hospital 17 cases of SIRS were found (11.0%), and three cases of severe SIRS (1.9%), among which there was one case of severe SIRS with shock. There was no difference between the group of patients with and without SIRS, regarding the 29 clinical, epidemiological and pharmacological variables that were analyzed. A tendency for a higher frequency of SIRS in patients undergoing anesthesia by halogenated substances was observed, but without statistical significance (p>0.05).At the Campinas Heart Institute Hospital, the prevalence of SIRS was of 29.2%. In this second study, in addition to being similar to the reality of cosmetic surgeries of our country, because it was conducted in a private hospital not related to any university, we could rely on the leucocyte count, collected after surgery. After an exhaustive review of the medical literature, some possible confounding analysis factors were found, namely: inhalational anesthetics (nitrous oxide as the halogenated), propofol, epidural anesthesia, the breast tissue itself (in their anatomy physiology presents interfaces with the immune system) and the adipose organ (part of the constitution of the breast, it has endocrine functions and is ontologically linked to the immune system). When reviewing the type of surgery performed and the pathophysiology of sepsis, we found two other relevant issues: immunosuppression and activation of the coagulation cascade associated to SIRS could generate a population of women transiently more susceptible to infectious complications, Deep Vein Thrombosis (DVT) and Pulmonary Thromboembolism (PTE). Again, we reviewed the literature to address these issues, numerous references were found involving the inappropriate use of antibiotics for bacterial complications (superinfection) and articles describing the incorrect use of the protocols for prophylaxis of DVT / PTE. Conclusion: In cosmetic breast surgery there is an incidence of SIRS close to 30% ( when the four diagnostic criteria for SIRS are used) and an incidence of severe SIRS close to 2%. Moreover, a clinical case of SIRS was described in the postoperative of cosmetic breast surgery, which is present in the everyday routine of the professionals that work with these patients but has not previously been related in the medical literature. No association was found between SIRS and the analyzed risk factors
Mestrado
Clinica Medica
Mestre em Clinica Medica
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Silva, André Augusto Botêga. "Alterações funcionais de mitocondrias hepáticas na tolerância ao lipopolissacarídeo (LPS)". Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/5/5164/tde-03012018-110429/.
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O presente estudo tem por objetivo principal avaliar as alterações funcionais precoces de mitocôndrias hepáticas de ratos wistar submetidos ao estímulo de sepse através da técnica de ligadura cecal e punção (cecal ligation and puncture-CLP) e indução de tolerância ao lipopolissacarídeo (LPS) de Escherichia coli. As mitocôndrias exercem papel na alteração do metabolismo celular de pacientes sépticos. Os objetivos do presente trabalho foram: (1) padronizar a técnica de indução a tolerância para ratos wistar com LPS de E. coli (2) avaliar a função mitocondrial fosforilativa e oxidativa; (3) quantificar DNA mitocondrial em tecido hepático de animais submetidos à CPL e tolerância; (4) verificar a expressão dos genes responsáveis pela biogênese mitocondrial e replicação do DNA mitocondrial: nuclear respiratory factor (NRF-1), mitochondrial transcription factor A (TFAM) e peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1alfa); (5) avaliar a função dos complexos respiratórios I e IV. Os resultados encontrados no presente estudo revelaram que: (a) a taxa de mortalidade dos animais submetidos a tolerância foi de 10% quando submetidos à dose letal de LPS, enquanto a taxa de mortalidade dos animais controle foi de 100% quando submetidos à dose letal de LPS; (b) observou-se que o grupo do controle respiratório que recebeu doses controladas de LPS e foi submetido à CLP apresentou razão igual ao grupo Controle, sugerindo que a fosforilação oxidativa se manteve igual ao basal, enquanto o grupo que foi submetido ao procedimento de CLP sem indução a tolerância apresentou piora da razão do controle respiratório em relação ao grupo controle; (c) a quantificação de DNA mitocondrial mostrou-se maior nos animais submetidos a CLP sem prévia indução a tolerância, com igual aumento da expressão dos fatores de biogênese mitocondrial em relação aos demais grupos; (d) houve diferença significativa na avaliação da funcionalidade dos complexo I, porém o complexo IV se manteve igual em todos os grupos. Concluiu-se que a indução a tolerância altera positivamente a função mitocondrial em animais submetidos à CLPThe aim of this study was to evaluate the early functional alterations of hepatic mitochondria of wistar rats submitted to the stimulation of sepsis through the technique of cecal ligation and puncture (CLP) and induction of tolerance to lipopolysaccharide (LPS) of Escherichia coli. Mitochondria play a role in altering the cellular metabolism of septic patients. The objectives of the present study were: (1) to standardize the tolerance induction technique for wistar rats with E. coli LPS (2) to evaluate the mitochondrial phosphorylation and oxidative function; (3) quantify mitochondrial DNA in hepatic tissue of animals submitted to CPL and tolerance; (4) to verify the expression of genes responsible for mitochondria biogenesis and mitochondrial DNA replication nuclear mitochondrial biogenesis (NRF-1), mitochondrial transcription factor A (TFAM) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1alpha); (5) to evaluate the function of respiratory complexes I and IV. The results found in the present study revealed that: (a) the mortality rate of the animals submitted to tolerance was 10% when submitted to the lethal dose of LPS, whereas the mortality rate of the control animals was 100% when submitted to the lethal dose of LPS; (B) it was observed that the group receiving controlled doses of LPS and submitted to CLP presented a ratio equal to the control group, suggesting that oxidative phosphorylation remained the same at baseline, whereas the group that underwent CLP procedure without induction of tolerance presented worsening of the respiratory control ratio in relation to the control group; (C) the mitochondrial DNA quantification was higher in the animals submitted to CLP without prior tolerance induction, with an equal increase in mitochondrial biogenesis factors expression in relation to the other groups; (D) there was significant difference in the evaluation of the functionality of complexes I, but no difference in complex IV in all groups. It was concluded that induction of tolerance positively alters mitochondrial function in animals submitted to CLP
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Chevalier, Geoffroy. "Analyse de la variabilité de la fréquence cardiaque en cas de syndrome de réponse inflammatoire fœtale aigu isolé ou associé à une hypoxie : Étude expérimentale chez le foetus de brebis". Electronic Thesis or Diss., Université de Lille (2022-....), 2024. http://www.theses.fr/2024ULILS060.
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Introduction : L'infection foetale avec syndrome de réponse inflammatoire foetale (SRIF) pendant le travail est associée au risque de développer une septicémie néonatale, des troubles du développement neurologique, une paralysie cérébrale, voire un décès. Lorsque l’acidose se surajoute au SRIF pendant le travail, cela induit une situation à très haut risque pour le foetus. Les méthodes actuelles pour diagnostiquer le SRIF sont insuffisantes. Nous avons émis l'hypothèse que l'analyse de la variabilité de la fréquence cardiaque foetale (VFC) pourrait être utilisée pour détecter le SRIF. Par conséquent, le premier objectif de notre travail était d'explorer si la VFC se modifiait au cours d’un SRIF. Le second objectif était d'étudier les changements de la VFC pendant une hypoxie progressive associée à un SRIF, en comparaison à une hypoxie isolée.Matériel et méthodes : Le modèle de SRIF était obtenu par l’injection de lipopolysaccharide (LPS) par voie intraveineuse à des foetus de brebis instrumentés, proches du terme. Un groupe témoin recevait une injection de sérum physiologique. Les paramètres hémodynamiques, les gaz du sang, le dosage d’interleukine-6 (IL-6) et 14 indices de VFC étaient enregistrés pendant six heures. Des comparaisons étaient faites entre les groupes LPS et le groupe témoin toutes les heures. Pour le second objectif, deux autres groupes ont été comparés : l’un avec une hypoxie isolée, l'autre avec une hypoxie associée à un SRIF. L'hypoxie progressive était induite par des occlusions répétées du cordon ombilical d’une minute pendant trois phases d’occlusions : légères, modérées et sévères. Les paramètres hémodynamiques et gazométriques ainsi que la VFC étaient comparés entre les groupes.Résultats : Concernant le premier objectif, 15 agneaux ont été instrumentés. Dans le groupe LPS (n = 8), l'IL-6 augmentait significativement après l'injection de LPS (p < 0,001), confirmant ainsi le modèle SRIF. La fréquence cardiaque foetale augmentait significativement à partir de H5 (p < 0,01). Cinq mesures de la VFC étaient significativement différentes entre le groupe LPS et le groupe témoin (le SDNN (déviation standard des intervalles NN / Standard Deviation of Normal to Normal), la SD2 (déviation standard 2 / Standard Deviation 2), le DFA (analyse des fluctuations sans tendances / Detrended Fluctuation Analysis) alpha 1 et 2 et la VLT (Variabilité à Long Terme). Concernant le second objectif, la mortalité était plus élevée dans le groupe hypoxie + SRIF (n = 4/9) en comparaison au groupe hypoxie isolée (n = 0/9). L'état gazométrique était modifié plus tôt en cas d’hypoxie associé au SRIF. Après les occlusions légères, le pH était significativement plus bas (7,22 [7,12-7,24] vs 7,28 [7,23-7,34], p = 0,01) et les lactates étaient significativement plus élevés (10,3 mmol/L [9,4-11,0] vs 6,0 mmol/L [4,1-8,2], p <0,001) dans le groupe hypoxie + SRIF. Après les occlusions légères, six indices de VFC étaient significativement augmentés dans le groupe hypoxie + SRIF en comparaison au groupe hypoxie isolée (le SDNN, le RMSSD (racine carrée de la moyenne des carrés des différences entre intervalles NN successif / Root Mean Square of Successive Differences), la VCT (Variabilité à court terme), la VLT, les LF (basses fréquences / Low Frequencies) et les HF (hautes fréquences / High frequencies)). Après les occlusions modérées, le SDNN et le RMSSD restaient significativement augmentés.Conclusion : Au cours d'un SRIF aigu, isolé ou associé à une hypoxie, la VFC est significativement modifiée. Ces changements semblent être médiés par une augmentation de la variabilité globale et une perte de complexité de la VFC. Ainsi, la VFC pourrait être utilisée pour la détection précoce de ces deux situations à risqueIntroduction: Fetal infection during labor, accompanied by fetal inflammatory response syndrome (FIRS), is linked to neurodevelopmental impairments, cerebral palsy, neonatal sepsis, and even mortality. Existing diagnostic methods for FIRS remain insufficient. Acidosis associated with FIRS during labor presents a significant risk to the fetus. This study hypothesizes that analysing fetal heart rate variability (HRV) could serve as a tool for detecting FIRS. Therefore, the first study aim was to explore whether fetal HRV change during FIRS and the second aim was to explore how HRV changes during acute FIRS-associated hypoxia, compared to isolated hypoxia. Material and methods: In near-term fetal sheep with chronic instrumentation, lipopolysaccharide (LPS) was administered intravenously to simulate FIRS, while a control group received an injection of saline solution. Hemodynamic parameters, blood gas levels, interleukin-6 (IL-6), and 14 heart rate variability (HRV) indices were recorded during a stability period and for six hours after injection. For these different parameters, hourly comparisons were made between the LPS and control groups. For the second aim, two other groups were compared: one with isolated hypoxia, the other with hypoxia and FIRS. Worsening hypoxia was induced by repeated umbilical cord occlusions in three one-hour phases: mild, moderate, and severe. Hemodynamic, gasometric, and HRV parameters were compared between the groups. Results: For the first aim, a total of 15 lambs were instrumented. In the LPS-treated group (n = 8), IL-6 levels significantly increased following LPS administration (p < 0.001), validating the FIRS model. Additionally, fetal heart rate showed a significant increase after H5 (p < 0.01). Significant differences between LPS and control groups were observed between H2 and H4 for five HRV measures (Standard Deviation of Normal to Normal (SDNN), Standard Deviation 2 (SD2), Detrended Fluctuation Analysis (DFA) alpha 1 and 2 and Long-Term Variability (LTV)). The hypoxia and FIRS group had a higher mortality rate (n = 4/9) compared with isolated hypoxia group (n = 0/9). Gasometric state was altered earlier in the hypoxia and FIRS group after mild occlusions (pH = 7.22 [7.12–7.24] vs 7.28 [7.23–7.34], p = 0.01; lactate = 10.3 mmol/L [9.4–11.0] vs 6.0 mmol/L [4.1–8.2], p <0.001). After mild occlusions, the hypoxia and FIRS group had higher values for six HRV parameters compared with the hypoxia group (SDNN, Root Mean Square of Successive Differences (RMSSD), Short Term Variability (STV), LTV, Low Frequencies (LF) and High frequencies (HF). After moderate occlusions, only SDNN and RMSSD remained significantly higher. Conclusion: During acute FIRS, associated or not with hypoxia, HRV is significantly changed. These changes appear to be mediated by an increase of global variability and a loss of signal complexity. HRV indices may therefore be valuable for early detection in these two situations
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Arshid, Samina. "Avaliação do efeito do précondicionamento isquêmico no proteoma e fosfoproteoma de neutrófilos de ratos após isquemia/reperfusão". Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/5/5132/tde-18012017-142837/.
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Introdução: O trauma é um fenômeno que cursa com lesão tecidual, sendo que o trauma cirúrgico (TC) apresenta a referida lesão como consequência de um ato cirúrgico. A isquemia seguida de reperfusão (IR) é um evento comum em várias condições patológicas, bem como em diversos procedimentos cirúrgicos, principalmente transplantes. É frequente o desenvolvimento de lesões teciduais locais e remotas após trauma e após a I/R, parte de um fenômeno conhecido como síndrome da resposta inflamatória sistêmica (SRIS), frequentemente seguida pela falência de múltiplos órgãos (FMO). Estudos provaram o envolvimento do neutrófilo em tais síndromes como resultado da ação de enzimas proteolíticas secretadas a partir de grânulos citoplasmáticos, radicais livres produzidos por explosão respiratória e citocinas liberadas após a infiltração nos tecidos. Nesse contexto, foi provado que o pré-condicionamento isquêmico (PCI), definido como curtos episódios de isquemia precedendo a IR, protege contra essas lesões, com menor ativação de neutrófilos. No entanto, o conhecimento a respeito dos mecanismos operantes nos neutrófilos após o trauma cirúrgico, a isquemia seguida de reperfusão ou o pré-condicionamento isquêmico, ainda são preliminares. Objetivo: Analisar com maior profundidade o impacto dessas condições (TC, IR e PCI) no proteoma e fosfoproteoma do neutrófilo. Métodos: Foi realizada a análise de parâmetros hematológicos juntamente com a análise proteômica e fosfoproteômica de neutrófilos de ratos submetidos a TC, IR e PCI, comparados ao grupo controle. A análise proteômica foi realizada em sistema de nLC-MS/MS orbitrap de alto desempenho, usando marcação com iTRAQ, enriquecimento de fosfopeptídios e pré-fracionamento por HILIC. A análise estatística baseada em clusters utilizando scripts em R mostrou proteínas com abundância relativa diferencial em todas as condições. Resultados: A avaliação dos parâmetros hematológicos antes e depois de TC, IR e IPC demonstrou alterações no número, forma e tamanho de linfócitos, hemácias, plaquetas e, principalmente, neutrófilos (granulócitos). Observou-se um claro aumento na contagem de neutrófilos após TC e IR, sendo que tal aumento foi prevenido pelo PCI. Um total de 393 proteínas foram determinadas como reguladas para abundância relativa entre o grupo controle e o grupo TC. A maioria das proteínas encontradas como reguladas em comum nos grupos TC e IR estão relacionadas à apoptose (caspase-3), motilidade celular (PAK2), transdução de sinal (IL-5, IL-6 e TNF) e degradação pelo sistema proteassoma no neutrófilo. Maior produção de espécies reativas de oxigênio e disfunção da migração direcional de neutrófilos (PKC-delta) com aumento do tempo de vida dos neutrófilos são eventos iniciais importantes que podem resultar em mais dano tecidual e em infecção. A análise proteômica de neutrófilos de ratos após PCI levou à identificação de 2437 grupos de proteínas atribuídos a 5 clusters diferentes, contendo proteínas de abundância relativa significativamente aumentada ou diminuída em IR e PCI. O estudo de vias desses clusters baseado no KEGG revelou aumento nas vias de fagocitose mediada por Fc-gama R, sinalização por quimiocinas, adesão focal e migração transendotelial, citoesqueleto de actina, metabolismo e diminuição nas vias ribossomais, de transporte de RNA, de processamento de proteínas. A regulação da fosforilação de proteínas após IR e PCI mostrou algumas vias como quimiocinas, Fc-gama, GPCR, migração celular e vias pró e antiapoptóticas, sendo que a via de splicing alternativo foi a que apresentou regulação mais evidente (p < 0.0001). A regulação da abundância, bem como da fosforilação, presença de motivos e de domínios levou à identificação de fosfatases, como Fgr, GRK2, PKC delta, ptpn6 e ptprc reguladas por IR, bem como stk38, pkn1, syk e inpp5d reguladas por PCI. A interação mais marcante entre proteínas foi demonstrada como sendo entre os receptores de Fgr e Ptp. Conclusão: Concluímos que as alterações causadas por TC, IR e PCI levaram a intenss alterações na abundância de algumas proteínas e em eventos de fosforilação em neutrófilos, levando ao efeito destrutivo observado após a IR e ao efeito protetor consequente ao PCIIntroduction: Trauma is a phenomenon that involves tissue injury, whereas the surgical trauma (ST) has such injury as a consequence of a surgery. Ischemia reperfusion is common event in many surgical procedures, especially in transplants, as well as in many pathological conditions. Local and remote tissue injuries usually develop after trauma and ischemic reperfusion, part of a phenomenon known as systemic inflammatory response syndrome, frequently followed by multiple organ failure (MOF). Studies have proven the involvement of the neutrophil in all these injuries as a result of proteolytic enzymes secreted from cytoplasmic granules, free radicals produced by respiratory burst, cytokines released after tissue infiltration. In that context, ischemic preconditioning (IPC), that are short episodes of ischemia before ischemia reperfusion, was proved to be protective against these injuries with less activation of neutrophils. However the knowledge about the underlying mechanism operating in the neutrophil after surgical trauma, ischemia reperfusion and preconditioning is preliminary. Objective: To deeply analyze the impact of these conditions (ST, IR and IPC) on the neutrophil proteome and phosphoproteome. Methodology: We did hematological analysis along proteomics and phospho proteomics through high throughput nLC-MS/MS analysis by orbitrap using iTRAQ labeling, phospho peptide enrichments, and HILIC pre-fractionation. Neutrophils from control, ST, IR and IPC conditions after extraction were processed for proteomic analysis. Statistical package using R based on cluster analysis led to the detection of differentially regulated proteins in all conditions. Results: The evaluation of the hematological parameters before and after ST, IR or IPC on blood cells stated alteration in size, number and shape of lymphocytes, RBCs, platelets and specially neutrophils (granulocytes). In the analysis, a clear increase in neutrophil count after ST and IR with such increase prevented by IPC. A total of 393 proteins were found differentially regulated between control and trauma groups. Most of the common proteins found regulated in trauma and IR seem to be related to apoptosis (caspase-3), cell motility (PAK2) and signal transduction in IL5, IL6 and TNF and proteasomal degradation in neutrophil. Higher oxygen species production and dysfunction of directional neutrophil migration (PKC delta) with increase in the life span of neutrophils are early important events that can finally result into more tissue damage and infection. The total proteomic analysis of rat neutrophils after IPC led to the identification of 2437 protein groups assigned to five different clusters with significantly up and downregulated proteins in IR and IPC. Cluster based KEGG pathways analysis revealed up-regulation of chemokine signaling, focal adhesion, leukocyte transendothelial migration, actin cytoskeleton, metabolism and Fc gamma R mediated phagocytosis, whereas downregulation in ribosome, spliceosome, RNA transport, protein processing in endoplasmic reticulum and proteasome, after intestinal ischemic preconditioning. The phosphoregulated proteins containing domains and motifs in the regulated peptides after IR and IPC led to the identification of some of important players such as chemokine, Fc gamma, GPCR, migration and pro/anti-apoptotic pathways. The phosphoproteins from alternative splicing was the pathway presenting the most remarkable regulation with a p-value of 0.0001. The regulation in expression as well as in phosphorylation, the presence of motifs and domains led to the identification of kinases and phosphatases including Fgr, GRK2, PKC delta, ptpn6 and ptprc in neutrophils after IR whereas stk38, pkn1, syk, and inpp5d in neutrophil due to IPC. The highest protein-protein interaction was shown by Fgr and Ptp receptors. Conclusion: We concluded that the changed stimulus produced after ST, IR and IPC led to the huge alteration in proteins expression and phosphorylation events in the neutrophil proteome as mentioned in our work, that leads to final destructive and protective phenotype of neutrophils respectively
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Ferreira, Cesar Augusto. "Efeitos da aprotinina em crianças com cardiopatia congênita acianogênica operadas com circulação extracorpórea". Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/17/17137/tde-11042010-210547/.
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Introdução. A Aprotinina parece reduzir o uso de transfusões, o processo inflamatório e o dano miocárdico, pós-CEC. Material e Métodos. Estudo prospectivo randomizado em crianças de 30 dias a 4 anos de idade, submetidas à correção de cardiopatia congênita acianogênica, com CEC e divididas em dois grupos, um denominado Controle (n=9) e o outro, Aprotinina (n=10). Neste, a droga foi administrada imediatamente antes da CEC. A resposta inflamatória sistêmica e disfunções hemostáticas e multiorgânicas foram analisadas por marcadores clínicos e bioquímicos. Foram consideradas significantes as diferenças com p<0,05. Resultados. Os grupos foram semelhantes quanto às variáveis demográficas e intra-operatórias, exceto por maior hemodiluição no Grupo Aprotinina. Não houve benefício quanto aos tempos de ventilação pulmonar mecânica, permanência no CTIP e hospitalar, nem quanto ao uso de inotrópicos e função renal. A relação PaO2/FiO2 (pressão parcial de oxigênio arterial/fração inspirada de oxigênio) apresentou queda significativa com 24 h PO, no Grupo Controle. Ocorreu preservação da concentração plaquetária com a Aprotinina enquanto no grupo Controle houve plaquetopenia desde o início da CEC. As perdas sangüíneas foram semelhantes nos dois grupos. No grupo Aprotinina surgiu leucopenia significativa, em CEC, seguida de leucocitose. Fator de necrose tumoral alfa (TNF-) , Interleucinas (IL)-6, IL-8, IL-10, proporção IL-6/IL-10, troponina I cardíaca (cTnI), fração MB da creatinofosfoquinase (CKMB), transaminase glutâmico-oxalacética (TGO) e fração amino-terminal do peptídio natriurético tipo B (NT-proBNP) não apresentaram diferenças marcantes intergrupos. A proporção IL-6/IL-10 PO aumentou no grupo Controle. A lactatemia e acidose metabólica pós-CEC foi mais intensa no grupo Aprotinina. Não houve complicações com o uso da Aprotinina. Conclusão. A Aprotinina não minimizou as manifestações clínicas e os marcadores séricos de resposta inflamatória sistêmica e miocárdicos, mas preservou quantitativamente as plaquetas.Introduction. Aprotinin seems to reduce the need for transfusion, the inflammatory process and myocardial damage after extracorporeal circulation (ECC). Material and Methods. A prospective randomized study was conducted on children aged 30 days to 4 years submitted to correction of acyanogenic congenital heart disease with ECC and divided into two groups: Control (n=9) and Aprotinin (n=10). In the Aprotinin Group the drug was administered immediately before ECC and the systemic inflammatory response and hemostatic and multiorgan dysfunctions were analyzed on the basis of clinical and biochemical markers. Differences were considered to be significant when P<0.05. Results. The groups were similar regarding demographic and intraoperative variables, except for a greater hemodilution in the Aprotinin Group. The drug had no benefit regarding time of mechanical pulmonary ventilation, permanence in the postoperative ICU and length of hospitalization, or regarding the use of inotropic drugs and renal function. The partial arterial oxygen pressure/inspired oxygen fraction ratio (PaO2/FiO2) was significantly reduced 24 h after surgery in the Control Group. Platelet concentration was preserved with the use of Aprotinin, whereas thrombocytopenia occurred in the Control Group since the beginning of ECC. Blood loss was similar for both groups. Significant leukopenia was observed in the Aprotinin Group during ECC, followed by leukocytosis. Tumor necrosis factor alpha (TNF-), interleukins (IL)-6, IL-8, IL-10, IL-6/IL-10 ratio, cardiac troponin I (cTnI), creatine kinase MB fraction (CKMB), glutamic-oxaloacetic transaminase (GOT) and the aminoterminal fraction of natriuretic peptide type B (NT-proBNP) ndid not differ significantly between groups.The postoperative IL-6/IL-10 fraction increased significantly in the Control Group. Post-ECC blood lactate concentration and metabolic acidosis was more intense in the Aprotinin Group. There were no complications with the use of Aprotinin. Conclusion. Aprotinin did not minimize the clinical manifestations or serum markers of the inflammatory, systemic and myocardial response, but quantitatively preserved the platelets.
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Albrecht, Madlin [Verfasser], e Ingo [Akademischer Betreuer] Ahrens. "The role of platelet immuno-receptors in patients with acute coronary syndrome and C-reactive protein induced pro-inflammatory gene response in early endothelial progenitor cells = Die Rolle von Plättchen Immuno-Rezeptoren bei Patienten mit akutem Koronarsyndrom und Einfluss von C-reaktivem Protein auf endotheliale Progenitorzellen". Freiburg : Universität, 2014. http://d-nb.info/1123481938/34.
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Islam, Md Hamidul. "Mathematical Modelling of the Inflammatory Response in Coronary Artery Disease". Thesis, Griffith University, 2017. http://hdl.handle.net/10072/365469.
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Atherosclerosis is a condition whereby fatty material is deposited in the walls of arteries resulting in a thickening of the wall. It is the leading cause of morbidity and mortality in much of the world, including Australia. Some of the clinical manifestations of atherosclerosis include acute ischaemic syndromes such as heart attacks and strokes. Despite continuous eorts over the past four decades, the biology of atherosclerosis and its clinical manifestations are still poorly understood. According to the response-to-injury hypothesis, this disease is initiated by an injury to or dysfunctionality of the inner lining of the artery (the endothelium) and progresses through multiple dynamical cell processes.
Mathematical models that take into account the initiation of atherosclerosis can be used to provide an integrated description of the mechanisms of the formation of an early atherosclerotic lesion. Such models may have signicant utility for designing future clinical and experimental studies, as well as in the development of therapeutic hypotheses and the provision of preventative advice for an individual or group of patients.
This thesis aims to develop models of the cellular dynamics of the process of early atherosclerosis, which will enhance the understanding of the cellular mechanics behind the formation of an early atherosclerotic lesion. In order to address the aims of the thesis, we present increasingly more realistic models.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Natural Sciences
Science, Environment, Engineering and Technology
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Rocha, Tais Sica da. "Marcadores de síndrome da resposta inflamatória sistêmica e sepse no pós-operatório de cirurgia cardíaca em crianças". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2012. http://hdl.handle.net/10183/77225.
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Objetivo geral: estudar a síndrome da resposta inflamatória sistêmica após a cirurgia cardíaca com circulação extracorpórea (CEC) e a sua relação com marcadores inflamatórios. Objetivos específicos: 1) avaliar a prevalência de síndrome da resposta inflamatória sistêmica (SIRS), sepse e disfunção de múltiplos órgãos (DMO); 2) avaliar a relação da SIRS, sepse e DMO com certos biomarcadores; 3) avaliar a relação desses biomarcadores com mortalidade no pós-operatório de cirurgia cardíaca com CEC em crianças; 4) estudar a cinética do soluble triggering receptor on myeloid cells-1 (sTREM-1), procalcitonina (PCT), proteína C reativa (PCR) neste grupo; 5) comparar os níveis séricos de sTREM-1, PCT e PCR entre pacientes sépticos e com SIRS. Desenho: estudo de coorte retrospectivo e prospectivo. Setting: unidade de terapia intensiva cardiológica (UTIC). Medidas: saturação venosa central de oxigênio, lactato arterial, glicose sérica, dosagem de troponina I, contagem total de leucócitos no sangue periférico, PCR, presença de SIRS, sepse e DMO foram avaliados nos cinco primeiros dias de pós-operatório na coorte retrospectiva. Na coorte prospectiva as amostras foram colhidas no préoperatório, na chegada à unidade de tratamento intensivo, no primeiro (1PO), segundo (2PO) e terceiro (3PO) dias de pós-operatório para dosagem específica de sTREM-1, PCT e PCR. Resultados: A coorte retrospectiva incluiu 121 pacientes com mediana de idade de 9 meses [IQ 4-75], de peso de 7Kg [IQ 4,3-14,7], de tempo de circulação extracorpórea de 56 minutos [IQ 43-81] e de clampeamento aórtico de 27 minutos [IQ15,2-51,7]. A mediana de tempo de internação em UTIC foi de 4 dias [IQ 2-8]. Os defeitos septais foram os mais frequentemente encontrados em 48% (58), seguidos de Tetralogia de Fallot. As taxas de mortalidade e de sepse neste grupo foram de 7,4% (9) e 27,7% (33) respectivamente. SIRS esteve presente em 50,8% (61) e DMO em 22,3% (27) na chegada da UTI. A presença de SIRS não infecciosa e DMO não relacionada à sepse foram mais frequentes em todos os dias de pósoperatório. O risco de mortalidade foi avaliado e sepse no 1PO teve o maior odds ratio (OR) = 31,71 (IC95: 2,6-393,8), seguido da presença de disfunção renal no 3PO, OR = 14,1 (IC95: 2,9 -66,6). A glicose sérica nas 6 horas de PO com OR = 2,4 (IC95: 1,03-5,7), a saturação venosa central de oxigênio do 1PO com OR = 12,2 ( IC95: 2,6-55,7) bem como o lactato arterial do 1PO com OR = 24,1 ( IC95: 4-112) mostraram-se com melhores poderes discriminativos para sepse, DMO e mortalidade respectivamente. Na coorte prospectiva foram incluídos 31 pacientes com medianas de idade de 11 meses [IQ 6-42], de peso de 8,1Kg [IQ 6-14], de tempo de CEC de 58 minutos [IQ 45-84], de clampeamento de 32 minutos [IQ 32-32] e de temperatura durante a CEC de 31ºC. A mediana de tempo de internação na UTI foi de 7 dias [IQ2-8]. Os defeitos septais foram os mais frequentes em 54,8% (17), seguidos da Tetralogia de Fallot. Ocorreram 6,5% (2) de óbitos e 12,7%(4) de sepse. A SIRS esteve presente em 45,8%(14) na chegada da UTIC. Observou-se elevação significativa dos níveis séricos de sTREM-1, PCT e PCR após a CEC. Os níveis medianos de sTREM-1 e da PCR estão acima dos níveis normais em todos os momentos avaliados, sendo a mediana do sTREM-1 de 143,6 pg/ml no préoperatório; de 96,9 pg/ml após a CEC; de 140,2 pg/ml após 24h da CEC; de 191,5 pg/ml após 48h (p < 0,05); e, de 193,3 pg/ml após 72h. Os níveis medianos de PCT estão acima dos normais somente no 3PO, considerando-se um ponto de corte de 0,5 ng/ml. Comparando-se os níveis medianos de PCR, PCT e sTREM-1 entre sépticos e não infectados não houve diferença significativa. Conclusões: Durante a primeira semana de pós-operatório de cirurgia cardíaca com CEC em crianças a presença de febre/hipotermia bem como de leucocitose está mais frequentemente relacionada à SIRS não infecciosa do que à sepse. Existe associação de mortalidade com sepse, síndrome de baixo débito e disfunção cardíaca, respiratória e renal tardias neste grupo. Os achados em relação à cinética da PCR e PCT confirmam os dados da literatura: diminuição dos níveis em 48h pós CEC. Os achados são originais em relação à cinética do sTREM-1. Não houve diferença nos niveis séricos de sTREM-1, PCT e PCR entre sépticos e não infectados, entretanto novos estudos são necessários devido à amostra pequena.Main objective: To study the systemic inflammatory response syndrome after cardiac surgery with cardiopulmonary bypass (CBP) and its relationship with inflammatory markers. Secondary objectives: 1) To assess the prevalence of Systemic Inflammatory Response Syndrome (SIRS), sepsis and multiple organ dysfunction syndrome (MODS); 2) to evaluate the relationship of systemic response syndrome (SIRS), sepsis and multiple organ dysfunction with certain biomarkers, 3) to evaluate the relationship of these biomarkers with mortality after cardiac surgery with cardiopulmonary bypass (CPB), 4) to study the kinetics of sTREM-1, procalcitonin (PCT), C-reactive protein (CRP) in this group 5) compare serum sTREM-11, PCT and CRP in patients with sepsis and systemic inflammatory response syndrome. Design: prospective and retrospective cohort. Setting: cardiac pediatric intensive care unit. Measurements: venous oxygen saturation (SvcO2), arterial lactate, glucose, troponin, total leukocyte count and C reactive protein, presence of systemic inflammatory response syndrome (SIRS), sepsis and multiple organ dysfunction syndrome (MODS) were evaluated in the first 5 post-operative days. The samples of the prospective study were taken in the pre-operative period, on arrival in the intensive care unit, and on the first (POD1), second and third post-operative days for dosing CRP, PCT and sTREM-1. Main results: The retrospective cohort included 121 patients with a median age of 9 months [IQR: 4-75] ,median weight of 7Kg [IQR: 4.3-14.7] , median CPB time of 56 minutes [IQR:43-81], median clamping time of 27 minutes [IQR: 15.28-51.75]. The median ICU stay was 4 days [IQR:2-8]. Septal defects were the most frequent, reaching 48% (58), followed by Tetralogy of Fallot. Mortality and sepsis rate was 7.4% (9) and 27.7% (33) respectively. SIRS was present in 50.8% (61) and MODS in 22.3% (27) at the ICU arrival. The presences of non-infectious SIRS and of non-sepsis-related MODS were also more frequent throughout the postoperative days. Mmortality risk was assessed, and sepsis in the first postoperative day had the highest odds ratio (OR) = 31.71 [CI95: 6 to 393.8], followed by renal dysfunction on the third day, OR = 14.1 [CI95: 2.9 to 66.6]. The 6hPO glucose with OR = 2.4 [CI95: 1.03 to 5.7], the SvcO2 POD1 with OR = 12.2 [CI95: 2.6 to 55.7] and POD1 lactate with OR = 24.1 [CI95: 4-112] showed better discriminative power for sepsis, MODS and mortality respectively. The prospective cohort included 31 patients with a median age of 11 months [IQR: 6-42], median weight of 8.1Kg [IQR: 6-14], median CPB time of 58 minutes [IQR: 45-84], median clamping time of 31 minute [IQR: 21-50] and median temperature of 32°C during CPB [IQR: 32-32]. The median ICU stay was 7 days [IQR: 2- 9]. Septal defects were the most frequent, at 54.8% (17), followed by Tetralogy of Fallot. Mortality rate was 6.5% (2) and incidence of sepsis was 12.7% (4). Systemic inflammatory response syndrome (SIRS) was present in 45.8% (14) of cases upon arrival at the ICU. We observed significant elevation of serum sTREM-1, PCT and CRP after CPB. The median levels of sTREM-1 and CRP levels are above normal levels at all time points evaluated with a sTREM-1 median of 143.6 pg/ml preoperatively, of 96.9 pg / ml after CPB, of 140.2 pg/ml after 24 hours of CPB, of 191.5 pg/ml after 48 h (p < 0.05) and 193.3 pg/ml after 72 h. Median PCT levels are above normal only in 3PO, considering a cutoff of 0.5 ng/ml. Comparing the median serum levels of CRP, PCT and sTREM-1 between septic and uninfected no significant difference was found. Conclusions: During the first week post-cardiac surgery with cardiopulmonary bypass in children the presence of fever / hypothermia and leukocytosis is more often related to non-infectious SIRS than sepsis. There is an association of mortality with sepsis, low output syndrome and cardiac dysfunction, and later renal and respiratory dysfunction in this group. The findings in relation to the kinetics of CRP and PCT confirm preview literature: decreased levels in 48 hours after CPB. The findings are unique compared to the kinetics of sTREM-1. There was no difference in serum levels of sTREM-1, PCT and CRP between septic and uninfected, however further studies are needed due to the small sample.
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Suppa, Alessandra Paes. "Estudo da expressão dos genes regulatórios de hipóxia durante a inflamação pulmonar produzida pela isquemia e reperfusão intestinal em camundongos AIRmax e AIRmin". Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/87/87131/tde-29042010-103419/.
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Homeostase do O2 é essencial para a sobrevivência e desenvolvimento fisiológico dos organismos. A falta de O2 nos tecidos é um fator subjacente comum na morbidade e mortalidade de situações clínicas como na Síndrome do Desconforto Respiratório Agudo (ARDS). Na retomada da homeostase as células mielóides exercem suas funções especializadas nas áreas de hipóxia. A adaptação destas células nesta condição depende dos produtos do gene HIF-1α, fator de transcrição que responde às mudanças de O2. Neste trabalho caracterizamos os mecanismos celulares e moleculares operantes no estado de hipóxia em resposta à reação inflamatória aguda no pulmão induzida pela I/R ateria mesentérica em duas linhagens de camundongos geneticamente selecionadas para máxima (AIRmax) ou mínima (AIRmin) Resposta Inflamatória Aguda (AIR). Observamos uma alta reação inflamatória aguda em resposta a I/R. Altos níveis de expressão dos genes envolvidos em situações de hipóxia Hif-1α, Vhl e das citocinas Il-1β e Il-6 mostraram-se relacionados com a alta AIR nos camundongos AIRmax.Oxygen homeostasis is essential for survival and physiologic development of organisms. Lack of O2 in tissues is a common underlying factor in morbidity and mortality for numerous serious medical conditions such as the Acute Respiratory Distress Syndrome (ARDS). For homeostasis recovery the myeloid cells exert their functions in specialized areas of hypoxia. The adaptation of myeloid cells in low O2 tissue depends on the HIF-1α gene products. Hif-1α is a transcription factor that responds to O2 levels change. In this study we characterize, in two lines of mice selected for maximal (AIRmax) or minimal (AIRmin) Acute Inflammatory response (AIR), the cellular and molecular mechanisms operating in the hypoxia state during an acute inflammatory reaction in the lung parenchyma produced by mesenteric artery Ischemia. We observed an acute inflammatory reaction with high levels of Hif-1α and Vhl genes expression involved in hypoxia conditions and IL-1β and IL-6 genes showed related to high AIR in AIRmax mice.
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Chimabucuro, Wilson Kohama. "Isquemia mesentérica e reposição do volume intravascular. Estudo comparativo entre duas soluções salinas com diferentes concentrações de cloreto de sódio nos eventos desencadeados pela reperfusão intestinal. Um modelo experimental em ratos". Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/5/5159/tde-10062010-143136/.
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A isquemia do intestino delgado ocorre nas oclusões arteriais dos vasos mesentéricos ou associada à baixa perfusão tecidual causada por choque circulatório. Seus efeitos deletérios locais e sistêmicos frequentemente agravam a evolução clínica de muitas doenças. Este estudo experimental investiga como a reposição do volume intravascular utilizando duas soluções salinas com diferentes concentrações de sódio (solução salina fisiológica e solução 7,5% de cloreto de sódio) modifica a resposta inflamatória e o estresse oxidativo causados pela isquemia do intestino delgado. Ratos Wistar, machos, peso corporal entre 250 e 300 g, número total =102, foram submetidos à oclusão transitória da artéria mesentérica superior durante 45 minutos. No protocolo utilizado, os animais foram sorteados para inclusão em um de quatro grupos experimentais: isquemia falsa (IF), isquemia intestinal seguida da infusão de solução salina hipertônica 7.5% em volume de 4 ml/kg de peso (SH), isquemia intestinal seguida da infusão de solução salina 0.9% em volume de 33 ml/kg de peso (SF) e isquemia intestinal sem reposição do volume intravascular (ST). Quando apropriado, as soluções foram administradas lentamente (5 minutos) pela veia jugular externa imediatamente antes da reperfusão intestinal. Em cada grupo experimental, logo após a reperfusão intestinal, os animais foram sorteados para tempo de sobrevida: 2 horas, 4 horas ou 6 horas após a reperfusão. Amostras de sangue foram colhidas pela veia jugular externa em vários períodos: imediatamente após a liberação da oclusão da artéria mesentérica, 2 horas, 4 horas e 6 horas após a reperfusão intestinal. O plasma foi separado e foram realizadas as dosagens de interleucinas (IL-6 e IL-10). No tempo determinado, os animais foram submetidos à eutanásia em condições humanamente aceitáveis e, então, nesse momento, foram colhidas amostras de tecidos (intestino, fígado e pulmão) para posterior quantificação das concentrações de malondialdeído (MDA) e interleucinas (IL-6 e IL-10). A atividade da mieloperoxidase (MPO) também foi avaliada nessas amostras. Os animais que não receberam tratamento apresentaram uma taxa de mortalidade maior do que os demais grupos. Os grupos de animais tratados com reposição de volume intravascular apresentaram uma taxa de mortalidade semelhante ao grupo de isquemia falsa. Os animais que receberam reposição de volume intravascular com soluções cristalóides (SH ou SF) apresentaram concentrações de MDA, MPO, IL-6 e IL-10 nos tecidos (intestino, fígado e pulmão) comparáveis ao grupo de animais com isquemia falsa. Em todos os momentos, esses valores foram mais elevados no grupo que não recebeu tratamento. As concentrações plasmáticas da IL-6 e da IL-10 foram mais elevadas nos animais tratados com SH. As análises mostram que a simples abertura da cavidade abdominal causa um trauma cirúrgico relevante aos animais e é responsável pelas alterações observadas no grupo de isquemia falsa. Os resultados sugerem que a isquemia intestinal transitória (45 minutos) realizada por oclusão da artéria mesentérica superior em ratos representa um modelo experimental de moderada gravidade. Dessa maneira, o modelo é adequado aos estudos das alterações bioquímicas e celulares que ocorrem a curto, médio e longo tempo de sobrevida. Este estudo foi elaborado para análise dos fatores relativos ao estresse oxidativo e reação inflamatória que ocorrem nas primeiras horas que seguem a reperfusão intestinal. De uma maneira geral, os animais foram beneficiados pela reposição do volume intravascular com soluções cristalóides. A solução salina fisiológica foi utilizada em volume aproximadamente oito vezes superior à solução hipertônica 7,5% de cloreto de sódio. Comparativamente, a atenuação similar das respostas deletérias após a reperfusão intestinal atingida com o uso de menor volume da solução hipertônica 7,5% de cloreto de sódio representa um fator positivo para a mesma. Considera-se que a maior concentração plasmática das interleucinas (IL-6 e IL-10) encontrada nos animais tratados com solução hipertônica7,5% de cloreto de sódio esteja relacionada ao aumento de permeabilidade da microcirculação associado às soluções hipertônicasGut ischemia is responsible for both local and systemic deleterious events. Since reperfusion occurs in a previous ischemic superior mesenteric artery territory (SMA), a succession of harmful mechanisms begins in the luminal epithelium that quickly lengthens the limits of the intestinal tract. Depending on the extension of the intestinal system involved in the ischemic/reperfusion injury there will be severe repercussion to distant organs in response to SMA occlusion. Several diseases could be associated with variables degrees of intestinal ischemia. Even minor intensity of intestinal ischemia had deleterious systemic effects and often aggravates the clinical outcome of many diseases. Our study investigates how different forms of volume restoration could modify two important mechanisms of injury after intestinal ischemia: oxidative stress and inflammatory responses. Wistar rats (n=102) were submitted to transient superior mesenteric artery occlusion (SMAo). After randomization, animals were divided in four groups: Sham intestinal ischemia; infusion of small volume of 7.5% hypertonic saline (HS), or infusion of high volume of 0.9% saline (NS) just prior reperfusion, and animals that did not receive intra vascular volume treatment (NT). At sequential times, the animals were euthanatized and tissue samples (lung, liver, and intestine) were collected to Malondialdehyde (MDA) dosage and myeloperoxidase (MPO) activity. Also, sequential plasmatic concentration of IL-6 and IL-10 were done. Animals treated with both forms of volume infusion showed lower levels of tissue MDA, MPO, IL-6, and IL-10 than found in NT group. Plasmatic concentration of IL-6 and IL-10 were higher in animals treated with HS. Positive correlation was found between tissue concentration of IL-10 and IL-6. The mortality rate was similar between the treated rats and the group of sham ischemia. The mortality rate was higher in the non treated animals. In this rat model of transient intestinal ischemia, adequate maintenance of intravascular volemia decreases oxidative stress and synthesis of inflammatory markers. Small volume of 7.5% HS (4ml/Kg body weight) and high amounts of NS ( 33 ml/Kg body weight) had similar effects in attenuation of these responses. In this study, 7.5% HS attenuates deleterious effects found after intestinal ischemia with the main advantage of the smallest volume utilized when compared with NS solution. Plasmatic concentrations of IL-6 and IL-10 were higher in HS treated animals. This observation is supported by action of hypertonic/hyperosmotic solutions at the microcirculatory level. These solutions increase the local vascular permeability. This characteristic of 7.5% HS solution could facilitate the passage of the locally produced interleukin to the systemic circulation
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Carvalho, Luiz Sérgio Fernandes de 1986. "Influência da lipoproteína de alta densidade (HDL) e de seu metabolismo intravascular sobre a resposta inflamatória e função endotelial na fase aguda do infarto do miocárdio". [s.n.], 2015. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312490.
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Orientadores: Andrei Carvalho Sposito, Valéria Nasser FigueiredoTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: Introdução: A resposta de fase aguda (RFA) transforma a lipoproteína de alta densidade (HDL) em uma partícula disfuncional que pode favorecer o estresse oxidativo/inflamatório e disfunção da enzima óxido nítrico sintase endotelial (eNOS). Ao mesmo tempo, a modulação do metabolismo da HDL pela proteína de transferência de colesteril ester (CETP) parece estar associada a um potencial efeito anti-inflamatório durante a RFA relacionada a sepse. Embora esses mecanismos possam estar envolvidos na disfunção endotelial que se segue ao infarto do miocárdio com supra de ST (IMCSST), essas hipóteses nunca foram testadas em humanos. Método: Plasma foi obtido de pacientes consecutivos com IMCSST (n=116 a 180) nas primeiras 24 horas após o início dos sintomas (D1) e no 5o dia (D5), sendo utilizado para medir: proteína C reativa (PCR), nitrato/nitrito (NOx) e atividade de CETP. As lipoproteínas foram isoladas por ultracentrifugação de gradiente. A oxidabilidade de LDL co-incubada com HDL (HDLaoxLDL) e auto-oxidabilidade da HDL (HDLautox) foram medidas após a incubação com CuSO4. A atividade anti-inflamatória da HDL foi estimada pela secreção de VCAM-1 por células endoteliais da veia umbilical humana, após a incubação com TNF-?. Dilatação mediada por fluxo (FMD) foi avaliada no 30o dia (D30). Resultados: Entre os pacientes no 1o tercil de HDL-colesterol no D1 (<33mg/dL), o incremento de NOx entre D1 e D5 e a FMD ajustada para várias co-variáveis foram maiores do que naqueles no 2o (33- 42mg/dL) e 3o (>42mg/dL) tercis. Do D1 ao D5 houve redução no tamanho e no número de partículas de HDL, bem como aumento da HDLaoxLDL e HDLautox. A secreção de VCAM-1 após estímulo com TNF-? foi reduzida após co-incubação com HDL de voluntários saudáveis, de doentes com IM no D1 e D30, mas não para a HDL do D5. A oxidação da HDL foi medida pela concentração de TBARS em partículas de HDL isoladas, sendo observado aumento entre D1 e D5, e permanecendo elevado no D30. O aumento no conteúdo de TBARS na HDL foi associado com a atividade de CETP (r=0,72; p=0,014), FMD (r =-0,61; p=0,046) e HDL-C (r=0,83; p=0,004). Em paralelo, elevada atividade de CETP na admissão foi associado a menor FMD, menor biodisponibilidade de NOx e a maior incidência de morte súbita e infarto recorrente após 30 (OR=12,8; p=0,032) e 180 dias (OR=3,3; p=0,044). Conclusão: O IMCSST induz mudanças na composição química e função do HDL, bem como alterações na atividade enzimática da CETP que paralelamente contribuem para o aumento da oxidação de partículas de HDL, que se traduz em disfunção endotelial
Abstract: Introduction: Acute phase response (APR) turns high-density lipoprotein (HDL) into a dysfunctional particle that may favor oxidative/inflammatory stress and endothelial nitric oxide (NO) synthase (eNOS) dysfunction. Moreover, modulation of HDL intravascular metabolism by cholesteryl ester transfer protein (CETP) action has also been implicated as a potentially anti-inflammatory and thrombotic mechanism during APR. Although these mechanisms may be involved into endothelial dysfunction that follows acute ST-elevation myocardial infarction (STEMI), these assumptions have never been in investigated in humans. Method: Plasma was obtained in the first 24-hours after STEMI symptoms onset (D1) and after 5 days (D5) in consecutive patients (n=116 to 180), and then used to measure C-reactive protein (CRP), nitrate/nitrite (NOx) and CETP activity. Lipoproteins were isolated by gradient ultracentrifugation. The oxidizability of low-density lipoprotein incubated with HDL (HDLaoxLDL) and the HDL self-oxidizability (HDLautox) were measured after CuSO4 co-incubation. Anti-inflammatory activity of HDL was estimated by VCAM-1 secretion by human umbilical vein endothelial cells after incubation with TNF-?. Flowmediated dilation (FMD) was assessed at the 30th day (D30) after STEMI. Results: Among patients in the first tertile of admission HDL-Cholesterol (<33mg/dL), the increment of NOx from D1 to D5 and the FMD adjusted for multiple covariates were higher than in those in the second (33-42mg/dL) or third (>42mg/dL) tertiles, respectively. From D1 to D5, there was a decrease in HDL size and particle number and increase in both HDLaoxLDL and HDLautox. VCAM-1 secretion after TNF-a stimulation was reduced after co-incubation with HDL from healthy volunteers, from MI patients at D1 and D30 but not from D5. Oxidized HDL was measured by TBARS in isolated HDL particles and increased from D1 to D5, and remaining elevated at D30. The change in TBARS content in HDL was associated with CETP activity (r=0.72;p=0.014), FMD (r=-0.61;p=0.046) and HDL-C (r=0,83,p=0,004). High CETP activity at admission was associated lower FMD, lower NOx bioavailability and with the incidence of sudden death and recurrent MI at 30 days (OR 12.8;p=0.032) and 180 days (OR 3.3;p=0.044). Conclusion: STEMI induces changes in the chemical composition and function of HDL as well as changes in the enzymatic activity of CETP that in parallel contribute to increased oxidation of HDL particles, and thus inducing endothelial dysfunction
Doutorado
Patologia Clinica
Doutor em Ciências Médicas
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Rosario, Andre Loureiro. "Efeito da ressuscitação volêmica precoce na resposta inflamatória e no estresse oxidativo cardiovascular do choque séptico experimental". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-01122014-113948/.
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Os mecanismos fisiopatológicos associados aos efeitos benéficos da reanimação guiada pela saturação venosa mista de oxigênio (SvO2) durante a sepse não são claros. Nosso objetivo foi avaliar os efeitos de um algoritmo de reanimação guiado pela SvO2 incluindo fluidos, noradrenalina e dobutamina na hemodinâmica, resposta inflamatória e estresse oxidativo cardiovascular durante um modelo experimental que se assemelha clinicamente ao choque séptico. Dezoito porcos anestesiados e cateterizados (35-45 kg) foram submetidos à peritonite por inoculação fecal (0,75 g/Kg). Depois de permanecerem hipotensos, antibióticos foram administrados e os animais foram randomizados em dois grupos: controle (n=9), com suporte hemodinâmico visando pressão venosa central de 8-12 mmHg, débito urinário de 0,5 ml/kg por hora, e pressão arterial média acima de 65 mmHg; e grupo SvO2 (n=9), com os objetivos acima referidos, além de SvO2 acima de 65%. As intervenções duraram 12 hs e incluíram Ringer Lactato e norepinefrina (ambos os grupos) e dobutamina (grupo SvO2). A resposta inflamatória foi avaliada pela concentração plasmática de citocinas, expressão de CD14 de neutrófilos, geração de espécies reativas de oxigênio e apoptose. O estresse oxidativo foi avaliado pelas concentrações de nitratos no miocárdio e no plasma, a atividade miocárdica e vascular de NAD(P)H oxidase, conteúdo de glutationa do miocárdio e expressão de nitrotirosina. A reanimação guiada por SvO2 foi associada com melhor índice sistólico, oferta de oxigênio e diurese. A sepse induziu em ambos os grupos um aumento significativo na concentração de IL-6, nas concentrações de nitrato de plasma e diminuição persistente na expressão de CD14 em neutrófilos. A apoptose e a geração de espécies reativas de oxigênio por neutrófilos não foram diferentes entre os grupos. As estratégias de tratamento não alteraram significativamente os parâmetros de estresse oxidativo. Assim, uma abordagem destinada a otimizar a SvO2 durante a sepse melhora a hemodinâmica, porém sem qualquer efeito significativo sobre a resposta inflamatória e estresse oxidativo. Os efeitos benéficos associados a esta estratégia podem estar relacionados a outros mecanismos.The pathogenetic mechanisms associated to the beneficial effects of mixed venous oxygen saturation (SvO2)-guided resuscitation during sepsis are unclear. Our purpose was to evaluate the effects of an algorithm of SvO2-driven resuscitation including fluids, norepinephrine and dobutamine on hemodynamics, inflammatory response and cardiovascular oxidative stress during a clinically resembling experimental model of septic shock. Eighteen anesthetized and catheterized pigs (35-45 Kg) were submitted to peritonitis by fecal inoculation (0.75 g/Kg). After hypotension, antibiotics were administered, and the animals were randomized to two groups: control (n=9), with hemodynamic support aiming central venous pressure 8 to 12 mmHg, urinary output 0.5 ml/Kg per hour, and mean arterial pressure greater than 65 mmHg; and group SvO2 (n =9), with the goals above, plus SvO2 greater than 65%. The interventions lasted 12 h, and lactated Ringer\'s and norepinephrine (both groups) and dobutamine (SvO2 group) were administered. Inflammatory response was evaluated by plasma concentration of cytokines, neutrophil CD14 expression, oxidant generation, and apoptosis. Oxidative stress was evaluated by plasma and myocardial nitrate concentrations, myocardial and vascular NAD(P)H oxidase activity, myocardial glutathione content, and nitrotyrosine expression. Mixed venous oxygen saturation-driven resuscitation was associated with improved systolic index, oxygen delivery, and diuresis. Sepsis induced in both groups a significant increase on IL-6 concentrations and plasma nitrate concentrations and persistent decrease in neutrophil CD14 expression. Apoptosis rate and neutrophil oxidant generation were not different between groups. Treatment strategies did not significantly modify oxidative stress parameters. Thus, an approach aiming SvO2 during sepsis improves hemoynamics, without any significant effect on inflammatory response and oxidative stress. The beneficial effects associated with this strategy may be related to other mechanisms
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Beppler, Jaqueline. "Identificação de peptídeos de Escherichia coli capazes de inibir a própria fagocitose em sepse". Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5164/tde-06062016-084247/.
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Introdução: Sepse é uma síndrome complexa definida por resposta inflamatória sistêmica, de origem infecciosa e caracterizada por manifestações múltiplas que podem determinar disfunção ou falência de um ou mais órgãos ou sistemas. É a principal causa de morte em unidades de terapia intensiva em pacientes críticos e tem representado uma fonte constante de preocupação para os sistemas de saúde em todo o mundo, devido, principalmente, às taxas elevadas de morbimortalidade. O tratamento da sepse é um desafio e continua a ser uma tarefa difícil devido a inúmeros fatores interferentes. Um estudo do nosso grupo demonstrou que a Escherichia coli (E. coli) é capaz de se ligar CD16 de um modo independente de opsonina, levando a um aumento na resposta inflamatória e a inibição da sua própria fagocitose, por conseguinte, procurou-se identificar os peptídeos no proteoma da E. coli envolvidos neste cenário. Metodologia: Utilizando a metodologia de Phage Display, que consiste numa técnica de clonagem, que permite a expressão de diversas sequências de peptídeos na superfície de bacteriófagos, nós identificamos 2 peptídeos que obtiveram interação com CD16. Após a seleção dos peptídeos identificamos uma proteína de membrana de E.coli que possui alta similaridade com um de nossos peptídeos selecionados. Nós acreditamos que esta proteína de membrana possa estar envolvida no processo de evasão imune desenvolvida pela E.coli e parece ser um forte candidato como uma nova opção terapêutica para controlar infecções por E. coli. Conclusão: A identificação de proteínas capazes de induzir inibição de fagocitose, através do receptor CD16, pode ser usada como uma nova forma de tratamento da sepse, assim como explorada no tratamento de doenças autoimunesIntroduction: Sepsis is a complex syndrome defined by a systemic inflammatory response of infectious origin and characterized by multiple manifestations that can determine dysfunction/failure of one or more organs and systems. It is the leading cause of death in intensive care units and represents a major health problem around the world, mainly due to its high mortality and morbidity rates. The treatment of sepsis is challenging and remains a difficult task due to numerous interfering factors. A study from our group demonstrated that Escherichia coli (E. coli) is able to bind CD16 in an opsoninindependent manner, leading to an increase in the inflammatory response and inhibition of its own phagocytosis, therefore we sought to identify the peptides in the E. coli proteome involved in this scenario. Methods and Results: Using the Phage Display technique, which is a cloning technique that allows the expression of various peptide sequences on the surface of bacteriophages (phages) and selecting these on the basis of affinity for a target molecule, we identified two peptides that interact with CD16. Next, using bioinformatic tools, we found an E. coli membrane protein that has high similarity with one of our selected peptides. We believe this membrane protein is involved in the process of immune evasion developed by E. coli and it is a strong candidate as a new therapeutic option to control E. coli infections. Conclusion: The identification of proteins capable of inducing inhibition of phagocytosis through the CD16 receptor, can be used as a new treatment of sepsis, as well as exploited in the treatment of autoimmune diseases
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Garib, Ricardo Alexandre. "Efeito da administração parenteral de glutamina sobre a modulação da resposta inflamatória sistêmica, morbidade e mortalidade de ratos submetidos à pancreatite aguda". Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5168/tde-21012016-154946/.
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INTRODUÇÃO: Relatos conflitantes têm dificultado para se estabelecer o potencial benefício da glutamina (GLN) no tratamento de condições inflamatórias agudas. Nós avaliamos o efeito da infusão parenteral de GLN, prévia à pancreatite aguda (PA) experimental, nos mediadores inflamatórios, morbidade e mortalidade. MÉTODOS: Ratos Lewis (n = 131) receberam glutamina parenteral (grupo GG), solução salina (grupo SS ou controle), ou permaneceram sem infusão parenteral (grupo Sham) por 48h. Após este período, foi induzida PA por meio da injecção retrógrada de taurocolato de sódio no ducto pancreático. Sangue, amostras de pulmão, fígado, pâncreas e líquido ascítico foram colhidos a partir de 2, 12 e 24 horas após PA para avaliação das variáveis propostas (citocinas, hsp, histologia, amilase). Sessenta animais permaneceram vivos após PA para a análise da mortalidade em sete dias. RESULTADOS: A análise entre grupos não mostrou diferenças significativas nos níveis de citocinas (p > 0,05). Análise cinética dentro de cada grupo ao longo do tempo mostrou maior INF-y no grupo Sham e SS às 2h do que em 12h e 24h, maior IL-2 e inferior IL-10 no Sham, às 24h do que em 2h e 12h, e menor IL-10 no SS e GG em 24 h do que no tempo de 2h (p <= 0.05). O grupo GG exibiu maior expressão de HSP 90 no pulmão e no fígado do que no grupo Sham nos tempos de 2h e 12h, respectivamente; e maior expressão no fígado de HSP90 e HSP70 no grupo SS no tempo 12 horas (p < 0,01). O grupo Sham apresentou maior expressão de HSP 70 no pulmão e HSP 90 no fígado do que os outros grupos no tempo de 24h. Não ocorreram alterações na taxa de mortalidade. CONCLUSÕES: Em modelo de PA experimental induzida por taurocolato de sódio, o pré-tratamento com GLN parenteral melhorou o perfil dos mediadores inflamatórios, sem afetar a mortalidadeINTRODUCTION: Conflicting reports have hindered establish the potential glutamine (GLN) benefit in treating acute inflammatory conditions. We evaluated the effect of parenteral GLN infusion before experimental acute pancreatitis (AP), as systemic inflammation-reproducing model, on inflammatory mediators and mortality. METHODS: Lewis rats (n=131) received parenteral glutamine (GG group), saline (SS or Control group), or remained without parenteral infusion ( Sham group) for 48h. Thereafter, AP was induced by retrograde injection of sodium taurocholate into pancreatic duct. Blood, lung, liver and pancreas samples were collected from 2, 12 and 24h post-AP to assess serum cytokines levels, tissue HSP expression, histology and amylase. Sixty animals remained alive post-PA for seven-day mortality analysis. RESULTS: Punctual between-groups analysis did not show differences in cytokine levels (p > 0.05). Intragroup analysis over time showed higher INF-y in Sham and SS at 2h than at 12h and 24h, higher IL-2 and lower IL-10 in Sham at 24h than at 2h and 12h, and lower IL-10 in SS and GG at 24h than at 2h timepoint (p <= 0.05). GG group exhibited higher lung and liver HSP90 than Sham at 2h and 12h timepoints, respectively; and higher liver HSP90 and HSP70 than SS at 12h timepoint (p < 0.01). Sham group presented higher lung HSP70 and liver HSP90 than the others at 24h timepoint (p < 0.02). No changes occurred on mortality rate. CONCLUSIONS: In sodium taurocholate-induced PA model, pretreatment with parenteral GLN improved inflammatory mediator\'s profile, without affecting mortality
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Gürsoy, Dilek. "Die Bedeutung des Gerinnungs- und Komplementsystems bei der Ausbildung eines "systemic inflammatory response syndroms" (SIRS) nach Eingriffen mit Hilfe extrakorporaler Zirkulation (EKZ) /". Düsseldorf, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000254035.
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Georgieff, Roland. "Untersuchungen zum Verlauf von hämodynamischen und gasanalytischen Parametern während der isolierten hyperthermen Extremitätenperfusion mit Tumornekrosefaktor Alpha und Melphalan". Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2004. http://dx.doi.org/10.18452/15068.
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Fragestellung: Es wird untersucht, ob die isolierte hypertherme Extremitätenperfusion (ILP) mit TNF-alpha und Melphalan eine akute systemische inflammatorische Reaktion (SIRS) auslöst. Weiterhin soll der Einfluß von zwei verschiedenen total intravenösen Narkoseverfahren sowie der Zusammenhang der unabhängig voneinander bestimmten Meßgrößen Herzindex/Sauerstoffverbrauchsindex (HI/VO2I) und Sauerstoffverbrauchsindex/Sauerstoffangebotsindex (VO2I/DO2I) beim Entstehen eines SIRS analysiert werden. Methodik: 73 Patienten, die sich einer ILP mit TNF-alpha und Melphalan in Allgemeinanästhesie unterzogen, wurden in diese klinische, retrospektive Untersuchung eingeschlossen. Ein erweitertes kardiopulmonales Monitoring, bestehend aus kontinuierlicher Thermodilution, kontinuierlicher indirekter Kalorimetrie, invasiver Blutdruckmessung sowie arterieller und gemischtvenöser Blutgasanalysen ermöglichte die Analyse von hämodynamischen, metabolischen und gasanalytischen Parametern an 8 definierten Zeitpunkten im Verlauf der ILP mit TNF-alpha und Melphalan. 21 Patienten erhielten eine Narkose mit Etomidate/Midazolam/Sufentanil/Pancuroniumbromid (N1), und bei 52 Patienten wurde die Narkose mit Propofol/Remifentanil/Cis-Atracurium (N2) durchgeführt. Ergebnisse: Während der ILP mit TNF-alpha und Melphalan kam es bei folgenden Parametern zu signifikanten Veränderungen in der systemischen Reperfusionsphase gegenüber den Ausgangswerten vor der extrakorporalen Zirkulation: Herzfrequenz, Herzindex, Temperatur, Gesamtsauerstoffaufnahme, pulmonale Sauerstoffaufnahme, Sauerstoffangebot, systemischer Gefäßwiderstand, pulmonalarterieller Mitteldruck, kardiale Füllungsdrücke, gemischtvenöser Kohlendioxid- und Sauerstoffpartialdruck, arterieller Kohlendioxid- und Sauerstoffpartialdruck, gemischtvenöse Sauerstoffsättigung, arterieller und gemischtvenöser Sauerstoffgehalt sowie arterieller pH- und Laktatwert. Bezüglich der Narkoseverfahren zeigte die Narkose N2 versus N1 signifikant geringere Herzfrequenzen und Herzindices, sowie signifikant erhöhte pulmonalarterielle Mitteldrücke, pulmonale und systemische Gefäßwiderstände. Die Korrelationen von HI/VO2I und VO2I/DO2I sind in der prä-Bypass-Phase gering, nehmen im Verlauf der ILP zu und erreichen zum Zeitpunkt der systemischen Reperfusion jeweils ihren Maximalwert. Schlußfolgerungen: Die ILP mit TNF-alpha und Melphalan kann als dynamisches in-vivo Modell für das Entstehen einer SIRS-Reaktion aufgefaßt werden. Die inflammatorische Antwort ist in ihrem Ausmaß eher gering und erreicht nach Aufhebung der extrakorporalen Zirkulation mit systemischer Reperfusion der behandelten Extremität ihr Maximum. Die Überwachung der Teilkreisläufe, ein erweitertes hämodynamisches Monitoring sowie forcierte intravenöse Volumentherapie in der Reperfusionsphase lassen dieses Behandlungsverfahren für die Patienten in Allgemeinanästhesie sicher erscheinen. Beide beschriebenen Narkoseverfahren sind für diese operative Therapie geeignet. Der Zusammenhang von HI/VO2I sowie VO2I/DO2I ist im Verlauf der ILP gering, kann sich aber mit Zunahme der inflammatorischen Reaktion verstärken.objective: To determine whether the isolated hyperthermic limb perfusion (ILP) with tumor necrosis factor alpha (TNF-alpha) and melphalan causes an acute systemic inflammatory response syndrome (SIRS)? Also analysed will be the influence of two total intravenous anaesthesias and the correlation of independent measured values cardiac index/oxygen consumption index (HI/VO2I) and oxygen consumption index/oxygen delivery index (VO2I/DO2I). design: Retrospective review of hemodynamic, metabolic and blood gas values from 73 patients, undervented isolated hyperthermic limb perfusion of leg with TNF-alpha and Melphalan in general anaesthesia. methods: Cardiopulmonary monitoring consisted of continuous thermodilution, continuous calorimetry, arterial pressure and arterial as well as admixed blood-gas analyses. Values were measured on 8 time points in the course of ILP. In 21 patients anaesthesia was carried out with drug-combination of Etomidate/Midazolam/Sufentanil/Pancuroniumbromid (N1), and 52 patients were given anaesthesia with Propofol/Remifentanil/Cis-atracurium (N2). results: The following values changed significantly after limb-reperfusion compared with the baseline: heart rate, cardiac index, temperature, oxygen consumption, pulmonary oxygen consumption, oxygen delivery, systemic vascular resistance, mean pulmonary arterial pressure, precardial pressures, admixed carbon dioxide pressure, admixed oxygen pressure, arterial carbon dioxide pressure, arterial oxygen pressure, admixed oxygen saturation, arterial and admixed oxygen content as well as arterial pH- and lactat. conclusions: The isolated hyperthermic limb perfusion with TNF-alpha and melphalan may be used as a dynamic in-vivo model for the development of an SIRS. The inflammatory response is slight and reached the maximum after reperfusion of treated limb. Monitoring of the two circulations, extended cardiopulmonary monitoring and intravenous volumetherapie in the reperfusion time makes this cancer treatment in general anaesthesia safe. Both anaesthesia are suitable. The correlations of HI/VO2I as well as VO2I/DO2I are low in the beginning and rise with the increase of the inflammatory response.
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Hassen, Tiffany Alicia. "Systemic inflammatory response syndrome and sepsis in major vascular surgery". Thesis, 2006. http://hdl.handle.net/2440/69444.
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This study aimed to identify relationships between post-operative systemic inflammatory response syndrome (SIRS) and sepsis, and markers of immunological, neuroendocrine, nutritional and psychological status ; to examine relationships between psychological variables and neuroendocrine responses to surgery; and to identify differences in immunological and neuroendocrine responses to open abdominal aortic aneurysm (AAA) repair compared with endovascular aneurysm repair (EVAR). It was concluded that higher pre-operative CD11b may be associated with more severe SIRS following major vascular surgery. Lower fat free mass and skeletal muscle mass are associated with more severe SIRS after AAA repair. Neuroendocrine responses reflect rather than predict post-operative SIRS and sepsis. No relationships between psychological parameters and neuroendocrine reponses to surgery were identified. Robust evidence of a greater inflammatory response to open AAA repair than EVAR has clarified contradictory reports in existing literature.Thesis (M.S.) -- University of Adelaide, Dept. of Surgery, 2006
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Bien, Mauo-Ying, e 邊苗瑛. "Breathing Pattern Variability in Patients with Systemic Inflammatory Response Syndrome or Persistent Vegetative State". Thesis, 2004. http://ndltd.ncl.edu.tw/handle/79825846055512767205.
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博士國立陽明大學
生理學研究所
92
The breathing pattern in normal subjects displays a certain variability, which is maintained by a central neural mechanism, feedback loops of arterial chemoreceptors and lung vagal sensory receptors, and cortical influences. Deviations in breathing pattern variability from the normal level have been found in individuals in pathological conditions. Quantitative methods, including calculations of coefficients of variation, the Poincaré plot, and the spectral analysis have been applied to analyze the breathing pattern variability to serve as indicators of pathophysiological conditions in patients with respiratory diseases or weaning outcome in patients with respiratory failure. In order to investigate their clinical applicability to respiratory care, we took two groups of patients for study: the one was composed of the postoperative patients recovering from systemic inflammatory response syndrome (SIRS) / sepsis and the other was the group of patients in persistent vegetative state (PVS). The former group of patients was at the recovering stage of acute condition, whereas the latter was in the chronic condition of unusual breathing control. SIRS patients usually present rapid breathing pattern leading to hyperventilation that requires mechanical ventilation in acute phase, but can recover to normal. It is therefore worth to investigate whether that variability can serve as a potential predictor of their weaning outcome. The PVS patients have spontaneous breathing but show deficit in cerebral blood flow, O2 delivery to brain tissue, cortical influences, and feedback loops of visceral and somatic afferent. Their spontaneous breathing patterns have not been well characterized. To investigate whether breathing pattern variability can serve as a potential weaning predictor for postoperative patients recovering from SIRS, 78 mechanically ventilated SIRS patients who had undergone abdominal surgery were included when they were ready for weaning. They were divided into success (n = 57) and failure (n = 21) groups based upon their weaning outcome. Another 19 successfully weaned patients who had undergone abdominal surgery without SIRS were included as control group. Before weaning, tidal volume, total breath duration, inspiratory time, expiratory time, and peak inspiratory flow were continuously monitored for 30 minutes, when the patients received 5 cmH2O pressure support ventilation. After the trial was successfully completed, the patients were extubated. Successful weaning was defined as the free from the ventilator over 48 hours, whereas failure referred to as reintubation of mechanical ventilation within 48 hours of extubation. The coefficient of variation and two values of standard deviation (SD1 and SD2；indicators of the dispersion of data points in the plot) obtained from the Poincaré plot of 5 respiratory parameters were lower in the failure group than in the success and control groups; there were no differences between the latter 2 groups. The areas under the receiver operating characteristic curve of these variability indices were within the range of 0.73-0.80, indicating their predicative accuracy. These results show that small breathing pattern variability is associated with a high incidence of weaning failure in postoperative patients recovering from SIRS and this variability may potentially serve as a weaning predictor. We investigated the breathing patterns of 27 patients with persistent vegetative state (PVS) and 15 normal volunteers (the control). Tidal volume (VT), total breath duration (TTOT), minute ventilation (VE), oxygen saturation (SpO2), and end-tidal CO2 tension (PetCO2) were monitored for three 30-min periods breathing air, 100% O2, and air again. During breathing air, 15 PVS patients (the PVS-IB) exhibited irregular breathing (IB), whereas the other 12 (the PVS-OB) displayed oscillatory breathing (OB). Either the PVS-IB or PVS-OB maintained average values of VT, TTOT, VE, and SpO2 similar to those of the control. The PVS-OB, but not PVS-IB, displayed a significantly lower PetCO2 than that of the control suggesting hyperventilation. The VT, TTOT, VE, and PetCO2, but not SpO2, of the PVS-OB showed cyclic changes. The coefficients of variation (indices of respiratory variability) of VT, TTOT, and VI were: PVS-OB > PVS-IB > control. Spectral analysis of VT revealed that the PVS-OB had a central peak of power with a cycle duration of 45 ± 13 s. Chemical denervation of peripheral chemoreceptors by inhalation of 100% O2 did not affect the respiratory variability of the PVS-IB, but it significantly reduced the respiratory variability and prevented OB of the PVS-OB. The OB reappeared within 5-460 min after termination of O2 inhalation. We concluded that 1) PVS patients display respiratory instability in the form of either IB or OB and 2) brain damage, hyperventilation, hypocapnia, and / or dysfunction of peripheral chemoreceptors may contribute to the pathogenesis of OB, whereas the former presumably could be the cause of IB. In conclusion, the analysis of variability provides an alternative method to describe the difference between two breathing patterns, especially when the patient presents significant change in breathing pattern but without changing the mean values of breathing pattern parameters. From the study of the variability of breathing pattern, we can further understand the mechanisms of breathing control to make it as a tool for clinical assessment and an index of therapeutic effect for patients with respiratory disorders.
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Niu, Shuo. "Regulation Of Innate Immune Cell Response Under Sub-acute/Chronic Inflammatory Conditions". 2017. http://scholarworks.gsu.edu/biology_diss/191.
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Sub-acute/chronic inflammatory diseases are often associated with altered inflammatory response, leading to increased host vulnerability to secondary inflammatory challenges. In the first study, by employing streptozotocin (STZ)-induced diabetes in mice, we further investigate mechanisms leading to enhanced polymorphonuclear leukocytes (PMN) response under hyperglycemia. We show that existence of a proinflammatory state associated with broad increases of macrophages in various organs plays a dominant role in promoting PMN response in diabetic mice. Studies of PMN infiltration during zymosan-induced peritonitis reveal that hyperglycemia enhances PMN recruitment through increasing F4/80+ macrophages in the peritoneal cavity. Insulin reversal of hyperglycemia reduces peritoneal macrophage numbers and ameliorates PMN infiltration. Significantly increased macrophages are also observed in the liver, kidneys, and intestines under hyperglycemia, and are attributable to exacerbated nephropathy and colitis when respective inflammatory conditions are induced. We also find that significant monocytosis of inflammatory F4/80+Gr-1+ monocytes from the spleen and macrophage proliferation in situ synergistically contribute to the increased macrophage population under hyperglycemia. In conclusion, our results demonstrate that STZ-induced hyperglycemic/diabetic mice develop a systemic proinflammatory state mediated by broad infiltration of macrophages. In the second study, we focus on the identification of the carrier that binds to and delivers Shiga toxin 2(Stx2) to the target organ causing hemolytic uremic syndrome (HUS). By employing a murine HUS model through co-injection of LPS-Stx2, we show that, adoptive transfer of CD11b+ leukocytes, but not CD11b- leukocytes, RBC, platelets or plasma, isolated from mice with HUS induces HUS in healthy recipients. Interestingly, we find that LPS priming of mice significantly promotes CD11b+ leukocytes binding to Stx2. Compared to CD11b+ leukocytes from mice without LPS priming, CD11b+ leukocytes isolated from mice after LPS priming demonstrate higher frequencies of toxin binding and augmented potency to induce HUS. In sum, our results demonstrate peripheral CD11b+ myeloid leukocytes act as effective Stx2 carriers that deliver toxin to kidneys causing HUS and that LPS-induced inflammation enhances the carrier capacity and aggravates HUS.
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Peng, Chia-Lin, e 彭佳琳. "Sea Buckthron Leave extracts decrease Lipopolysaccharide-Induced systemic inflammatory response syndrome in C57BL/6 Mice". Thesis, 2013. http://ndltd.ncl.edu.tw/handle/39529333189384927727.
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碩士中山醫學大學
營養學研究所
102
Systemic inflammatory response syndrome (SIRS)is a serious and fatal disease in clinic. Lipopolysaccharide (LPS), derived from the cell wall of gram-negative bacteria, can induce a series of physiological or pathological changes resulting in septic shock and cause multiple organ dysfunctions. LPS-mediated endotoxinas well as a number of catabolic factors can cause severe inflammation and eventually lead to septic shock.Studies have shown that reactive oxygen species (ROS) is overproduced by the stimulation of LPS, and directly implicated as the second messengers in activation of NF-κB as well asmitogen-activated protein kinase (MAPK). Oxidants, free radicals and their derivatives also play important roles in the initiation and progression of skeletal muscle atrophy in various diseases states. The administration of antioxidants may attenuate myofiber atrophy in animal model. Muscle mass is the dynamic balance between the synthesis and degradation of muscle proteins. The rate of proteins degradation is more than biosynthesis which can cause muscle wasting.Two cellular proteolytic systems are involved in various of muscle atrophy including sepsis, which are the ubiquitin-proteasome pathway (UPP) and the autophagy- lysosomal pathway (ALP). Sea buckthorn (SBT, Hippophaerhamnoides Linn) is the popular herb used forcardiovascular diseases, mucosal injuries and skin disorders. Although the leaf extract of SBT have anti-bacterial, anti-viral and anti-tumor activities, the anti-muscle wasting effect of SBT leave is still unknown. In this study, we investigated the effects of water and ethanol extracts of SBT onLPS-induced muscle atrophy. Our results demonstrate thatmice was fed with water and ethanol extracts of SBT decreased LPS-induced skeletal muscle atrophy through theinhibition of UPP and ALP related atrophy-specific genes expression. Taken together, our findings suggest that SBT leave could prevent muscle wasting through the inhibition of UPP and ALP pathway.
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Pevec, Till [Verfasser]. "Dexamethason-21-isonicotinat als Begleittherapie bei Kühen mit Systemic Inflammatory Response Syndrome / eingereicht von Till Pevec". 2007. http://d-nb.info/986797782/34.
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