Relevant bibliographies by topics / Septic shock; Inhibitors

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Septic shock; Inhibitors'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Septic shock; Inhibitors.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Septic shock; Inhibitors"

1

Orlicek, Shari L. "Cytokine inhibitors for sepsis and septic shock." Seminars in Pediatric Infectious Diseases 12, no. 1 (January 2001): 24–29. http://dx.doi.org/10.1053/spid.2001.19232.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Cohen, J., and A. Silva. "NO inhibitors and septic shock." Lancet 339, no. 8795 (March 1992): 751. http://dx.doi.org/10.1016/0140-6736(92)90657-o.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Strukov, Danila Viktorovich, Andrey Glebovich Vasiliev, and Yuriy Stanislavovich Alexandrovich. "No inducible synthase inhibitors produce a positive effect on indexes of central hemodynamics in rats with septic shock." Pediatrician (St. Petersburg) 6, no. 4 (December 15, 2015): 45–50. http://dx.doi.org/10.17816/ped6445-50.

Full text
Abstract:
The purpose of the study was to evaluate the efficacy of NO inducible synthase (iNOS) inhibitors involved in simulation of septic shock in rats. Model of septic shock (SS) was obtained in rats by intravenous administration of live Bifidobacteria culture. Aminoguanidine was used as a selective inhibitor of iNOS. Indexes of central hemodynamics measured by direct method where analyzed. Vascular endothelial function was rated by determination of nitric oxide (II) (NO), vascular endothelial growth factor A (VEGF-A) and tissue plasminogen activator (tPA) in plasma. Hemostatic parameters were evaluated by the level of soluble fibrin monomer complexes (RKMF). Intravenous administration of live Bifidobacteria culture in rats proved to cause an adequate and effective septic shock model with characteristic changes of hemodynamics in laboratory animals, development of endothelial dysfunction and hemostasis system activation in response to bacteremia. INOS inhibitors have a positive impact on hemodynamics in septic shock. NO is not the only factor in the development of hypotension in septic shock. INOS inhibitors appear to affect the extent of vasopressor dose utilized in the therapy of septic shock contributing to improvement of microcirculation and tissue oxygenation.
APA, Harvard, Vancouver, ISO, and other styles
4

Martínez-Brotóns, F., J. R. Oncins, J. Mestres, V. Amargós, and C. Reynaldo. "Plasma Kallikrein-Kinin System in Patients with Uncomplicated Sepsis and Septic Shock-Comparison with Cardiogenic Shock." Thrombosis and Haemostasis 58, no. 02 (1987): 709–13. http://dx.doi.org/10.1055/s-0038-1645960.

Full text
Abstract:
SummaryAlterations of the kallikrein-kinin system consistent with activation and increased consumption have been re2ported in septic patients and it has been suggested that this activation could contribute to the development of septic shock.The aim of this work was to confirm these alterations in septic patients and to investigate the possible existence of similar changes in subjects developing cardiogenic shock secondary to myocardial infarction as a model of non septic shock.Patients with septic shock, especially in fatal cases, showed a highly significant decrease in levels of factor XII, prekallikrein, high molecular weight kininogen (HMW-kininogen), α2-macro-globulin (α2-M) and antithrombin III (AT-III). C1-esterase inhibitor (C1-INH) activity was increased in uncomplicated sepsis but came back to normal or was slightly decreased in septic shock.Components and inhibitors of the kallikrein-kinin system were within normal limits in patients with cardiogenic shock.Our findings support the idea of a contribution of the kallikrein-kinin system to the development of septic shock though this system does not seem to play a significant role in the pathogenesis of cardiogenic shock or seem to be altered as a consequence of it.
APA, Harvard, Vancouver, ISO, and other styles
5

Wearden, Mary E. "Nitric oxide synthase inhibitors for septic shock." Seminars in Pediatric Infectious Diseases 12, no. 1 (January 2001): 42–45. http://dx.doi.org/10.1053/spid.2001.19234.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Strukov, Danila Viktorovich, Yuriy Stanislavovich Alexandrovich, and Andrey Glebovich Vasiliev. "Actual aspects of sepsis and septic shock." Pediatrician (St. Petersburg) 5, no. 2 (June 15, 2014): 81–87. http://dx.doi.org/10.17816/ped5281-87.

Full text
Abstract:
He review presents an analysis of up-to-date views on sepsis and septic shock. Results of consenting conferences are given with classification of sepsis in adults and children. Mortality indexes are presented in patients’ group with sepsis. Basic pathogenesis links are examined i.e. bacteriemia, microbe toxemia, endo(auto)toxicosis, systemic destructive vasculitis, growing hypercoagulation transforming into coagulopathia, consumption trombocytopenia with trombohemorrhagic syndrome and severe immunesuppression. Pathogenesis of septic shock is divided into processes developing in various organs and tissues as well as into intracellular ones: such as oxidative stress and mitochondrial insufficiency. The role of pathogen-associated molecular images - patterns is portrayed in the development of generalized acyclic infection process. A scheme of up-to-date septic shock therapy is presented. An important role of nitrogen oxide in the development of stabile hypotonia resistant to vasopressin therapy is proven. The potency of nitrogen oxide to produce free-radical peroxinitrite inducing lipids peroxide oxidation in membranes is reflected. Its ability to react with non-hem iron- and zink- containing proteins is mentioned. Key factors contributing to activation of genes responsible for inducible nitrogen oxide synthase operation are revealed. Extremely severe sepsis and septic shock are believed to be the most serious problem of contemporary medicine thus necessitating to produce new medicines affecting the most drug-resistant links of its pathogenesis. In many a countries trials are continuing to introduce new medicines like nitrogen oxide synthase inhibitors for the treatment of patients with septic shock.
APA, Harvard, Vancouver, ISO, and other styles
7

Haj, Montaser A., Linda A. Robbie, Gillian D. Adey, and Bruce Bennett. "Inhibitors of Plasminogen Activator in Neutrophils and Mononuclear Cells from Septic Patients." Thrombosis and Haemostasis 74, no. 06 (1995): 1528–32. http://dx.doi.org/10.1055/s-0038-1649977.

Full text
Abstract:
SummaryLeucocytes, both polymorphs and mononuclear cells, play a variety of roles in the evolution of human response to sepsis, both local and generalised. In this study, inhibitors of plasminogen activator were measured in leucocytes from normal and septic patients. Plasminogen activator inhibitor-1 (PAI-1) was identified in polymorphs from normal individuals and levels rose significantly in polymorphs from septic patients: neutrophils from normal subjects did not contain PAI-2 but this protein was detectable in significant quantities in polymorph preparations from septic patients. In contrast, mononuclear cells from normal and septic patients contained no detectable quantities of PAI-1. Significant amounts of PAI-2 were present in normal mononuclear cells, and the levels rose significantly in monocytes from septic patients. PAI-2 is thus here identified in human subjects, distinct from those with pregnancy or malignancy, as playing a role in a pathological process. The increased levels of both inhibitors produced by leucocytes may clearly contribute directly to the persistence of fibrin, a characteristic feature of the response to infection, local or general; they may thus participate in successful localisation of infections (abscess formation etc.) and in the evolution of the major systemic complications of disseminated sepsis characterised by microvascular occlusion by fibrin such as renal failure, shock lung or digital ischaemia.
APA, Harvard, Vancouver, ISO, and other styles
8

Mesters, RM, PM Mannucci, R. Coppola, T. Keller, H. Ostermann, and J. Kienast. "Factor VIIa and antithrombin III activity during severe sepsis and septic shock in neutropenic patients." Blood 88, no. 3 (August 1, 1996): 881–86. http://dx.doi.org/10.1182/blood.v88.3.881.881.

Full text
Abstract:
Abstract Septic shock and multiple organ failure may be associated with coagulation activation, disseminated fibrin formation, and consumption of coagulation inhibitors such as antithrombin III. We have evaluated prospectively coagulation measurements in patients with severe chemotherapy-induced neutropenia. This group of patients was chosen because of their high risk of developing severe septic complications, thus allowing serial prospective coagulation testing before and during evolving sepsis or septic shock. Sixty-two patients with febrile infectious events were accrued to the study. Of these, 13 patients progressed to severe sepsis and 13 additional patients to septic shock as defined according to standard diagnostic criteria. At the onset of fever, factor (F) VIIa activity, FVII antigen and antithrombin III (AT III) activity decreased from normal baseline levels and were significantly lower in the group of patients who progressed to septic shock compared with those that developed severe sepsis (medians: 0.3 v 1.4 ng/mL, 21 v 86 U/dL and 45% v 95%; P < .001). The decrease of these measurements in septic shock was accompanied by an increase in prothrombin fragment 1+2 (median: 3.6 v 1.4 nmol/L; P = .05), a marker of thrombin generation. These differences were sustained throughout the septic episode (P < .0001). FVIIa and AT III levels of < 0.8 ng/mL and < 70%, respectively, at onset of fever predicted a lethal outcome with a sensitivity of 100% and 85%, and a specificity of 75% and 85%, respectively. In contrast, FXIIa-alpha antigen levels were not different between groups at onset of fever but increased modestly during the course of septic shock (P = .001). Thus, septic shock in neutropenic patients is associated with increased thrombin generation. Furthermore, both FVIIa and AT III measurements are sensitive markers of an unfavorable prognosis.
APA, Harvard, Vancouver, ISO, and other styles
9

Mesters, RM, PM Mannucci, R. Coppola, T. Keller, H. Ostermann, and J. Kienast. "Factor VIIa and antithrombin III activity during severe sepsis and septic shock in neutropenic patients." Blood 88, no. 3 (August 1, 1996): 881–86. http://dx.doi.org/10.1182/blood.v88.3.881.bloodjournal883881.

Full text
Abstract:
Septic shock and multiple organ failure may be associated with coagulation activation, disseminated fibrin formation, and consumption of coagulation inhibitors such as antithrombin III. We have evaluated prospectively coagulation measurements in patients with severe chemotherapy-induced neutropenia. This group of patients was chosen because of their high risk of developing severe septic complications, thus allowing serial prospective coagulation testing before and during evolving sepsis or septic shock. Sixty-two patients with febrile infectious events were accrued to the study. Of these, 13 patients progressed to severe sepsis and 13 additional patients to septic shock as defined according to standard diagnostic criteria. At the onset of fever, factor (F) VIIa activity, FVII antigen and antithrombin III (AT III) activity decreased from normal baseline levels and were significantly lower in the group of patients who progressed to septic shock compared with those that developed severe sepsis (medians: 0.3 v 1.4 ng/mL, 21 v 86 U/dL and 45% v 95%; P < .001). The decrease of these measurements in septic shock was accompanied by an increase in prothrombin fragment 1+2 (median: 3.6 v 1.4 nmol/L; P = .05), a marker of thrombin generation. These differences were sustained throughout the septic episode (P < .0001). FVIIa and AT III levels of < 0.8 ng/mL and < 70%, respectively, at onset of fever predicted a lethal outcome with a sensitivity of 100% and 85%, and a specificity of 75% and 85%, respectively. In contrast, FXIIa-alpha antigen levels were not different between groups at onset of fever but increased modestly during the course of septic shock (P = .001). Thus, septic shock in neutropenic patients is associated with increased thrombin generation. Furthermore, both FVIIa and AT III measurements are sensitive markers of an unfavorable prognosis.
APA, Harvard, Vancouver, ISO, and other styles
10

DeMott, Joshua M., Gourang Patel, and Ishaq Lat. "Effects of Chronic Antihypertensives on Vasopressor Dosing in Septic Shock." Annals of Pharmacotherapy 52, no. 1 (August 11, 2017): 40–47. http://dx.doi.org/10.1177/1060028017726552.

Full text
Abstract:
Background: In septic shock, chronic antihypertensive medications are held acutely. Vasopressors are often required to maintain blood pressure. The effect of chronic exposure to antihypertensive therapies on vasopressor dosing in septic shock is not known. Objective: To determine the effects of chronic exposure to antihypertensive therapies, specifically β-blockers and angiotensin-converting enzyme (ACE) inhibitors, on cumulative vasopressor dosing in septic shock. Methods: This was a retrospective cohort review, with data collected from routine care. Patients admitted to the medical intensive care unit with septic shock and vasopressor use were included and divided into 4 groups based on chronic medication use: (1) no β-blocker or ACE inhibitor, (2) β-blocker only, (3) ACE inhibitor only, and (4) β-blocker and ACE inhibitor. Cumulative vasopressor dose at 48 hours was assessed. Demographics, comorbid conditions, suspected site of infection, disease severity, mortality, and concomitant therapies were evaluated between groups. Results: A total of 133 patients with septic shock treated with vasopressors were included. No difference in cumulative vasopressor dose at 48 hours was detected between the 4 groups, respectively (median norepinephrine milligram equivalents [interquartile range (IQR)]: no β-blocker or ACE inhibitor, 13.7 mg [6.0-35.7]; β-blocker only, 13.1 mg [5.4-23.9]; ACE inhibitor only, 13.2 mg [1.2-36.7]; β-blocker and ACE inhibitor, 11.3 mg [4.7-42.9]; P = 0.669). Total time on vasopressors differed between groups (median hours [IQR]: no β-blocker or ACE inhibitor, 30h [17-60]; β-blocker only, 24h [10-69]; ACE inhibitor only, 19h [6-25]; β-blocker and ACE inhibitor, 30h [15-58]; P = 0.031). Comorbid conditions, suspected infection sites, disease severity, mortality, and concomitant therapies were similar. Conclusions: Chronic β-blocker, ACE inhibitor use, or the combination of both did not affect cumulative vasopressor dose at 48 hours in septic shock. However, prior-to-admission medications may affect total time of vasopressor use.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Septic shock; Inhibitors"

1

Bertsche, Joseph. "Histone Deacetylase Inhibitors and Innate Immunity in Septic Shock." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/2011.

Full text
Abstract:
Innate immunity depends on pattern recognition receptors, which recognize pathogen associated molecular patterns (PAMPS), such as Toll-like receptor 4 (TLR4), which detects the gram-negative bacterial toxin, lipopolysaccharide. Engagement of TLR4 by LPS sets off a cascade ending in the activation of pro-inflammatory cytokines and interferon-β (IFN-β) which alerts the host to the infection. However, these responses can be mal-adaptive, especially in the context of bacterial sepsis, where a "cytokine storm" results in death of the host. Pharmacological modulation of these responses may therefore be a promising treatment modality. Inhibition of classic pro-inflammatory cytokines such as IL-1β and TNF-α has been the (largely unfruitful) focus of much research. However it has recently emerged that mice with defects in type I IFN signaling are also substantially resistant to challenge with endotoxin. We therefore wish to investigate pharmacological inhibition of IFN signaling as a potential means to control sepsis. We analyzed the effects of Trichostatin A (TSA) and Suberoylanilide hydroxamic acid (SAHA) (both broad spectrum HDAC inhibitors) and ST-2-92 (HDAC6 specific inhibitor) on IFN regulation and endotoxic shock. We created an in vivo mouse model for this treatment with TSA and SAHA (which are well tolerated in mouse and human) to look for possible alteration in the survival rate following endotoxin challenge. We as well as others found that treatment with SAHA (50mg/kg) significantly improves survival rate. We also characterized in-vitro modulation of IFN responses through SAHA by mouse DNA microarray. We noticed a decreased expression of many innate immune regulated genes in the SAHA and LPS treated condition compared to the LPS treatment alone. Additionally we observed a decrease in protein levels of IFN-β IL-1β, IL-6, IL-12p40, RANTES and TNF-α in cell culture supernatants treated with SAHA or ST-2-92 and LPS compared to LPS only treatment. These results show the ability of broad spectrum HDACi through SAHA to increase mouse survival following LPS challenge as well as modulate the induction of innate immune responsive genes in vitro. Furthermore we have shown that HDAC specific inhibition through ST-2-92 can decrease pro-inflammatory transcript as well as protein levels.
APA, Harvard, Vancouver, ISO, and other styles
2

Clark, Megan Frances. "Effects of endotoxin on cationic amino acid transport in peripheral blood mononuclear cells." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298251.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Hjerdt-Goscinski, Gunilla. "Antibiotic-induced Bacterial Toxin Release – Inhibition by Protein Synthesis Inhibitors." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4692.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Pritts, Timothy A. "NUCLEAR FACTOR-KAPPA B ACTIVATION IN THE ENTEROCYTE AND INTESTINAL MUCOSA: REGULATION BY THE HEAT SHOCK RESPONSE AND PROTEASOME INHIBITORS." University of Cincinnati / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ucin990705885.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Lee, Jie-Jen, and 李居仁. "Inhibitory effect of therapeutic agent in LPS-induced septic shock in rats." Thesis, 2000. http://ndltd.ncl.edu.tw/handle/81925794698735851427.

Full text
Abstract:
碩士
台北醫學院
醫學研究所
88
Abstract Background Septicemia is generally caused by a cell wall component in Gram negative bacterias called lipopolysaccharide (LPS). It promotes the synthesis of nitric oxide (NO), which induces drastic blood pressure fall, tissue hypoperfusion, (a state known as “septic shock”), and even death. Objective and Methods To evaluate mechanisms of drugs commonly used in the treatment of septicemia, giving antibiotics including Minocycline (10 mg/kg), Clindamycin (10 mg/kg), Cyclosporin (15 mg/kg) and Platonin (10 mg/kg) to septicemic rat injected with LPS. Clinical improvement, blood pressure, heart rate, survival time are assessed, and the amount of endogenous NO production is determined. Difference between whether or not drug therapy was given, and possible causative factors were discussed. Results First of all, we choose minocycline (10 mg/kg), which has the ability of binding to the 30S of the ribosomes in the cytoplasm of the bacterial cell, inhibiting the synthesis of bacterial proteins. As a result, Minocycline blocks the hypotensive effect induced by LPSs, and at the same time, decreases the production of endogenous NO. Therefore, Minocycline’s blood-pressure stabilizing effect may be due to its inhibitory mechanism to the synthesis of NO. Clindamycin has the same affinity of binding to the 30S in bacterial ribosome. Giving this drug at the dose of 10 mg/kg, LPS-induced hypotension and the endogenous production of NO were effectively blocked simultaneously. We can conclude that both minocycline and clindamycin posses the same antimicrobial mechanism, effectively reversing the hypotensive phenomena induced by LPSs. Cyclosporin on the other hand, is a potent immunologic agent, acting as inhibitor of T-cell reactions, and of lymphokine production and its delivery. Our experiment showed that the administration of Cyclosporin (15 mg/kg) 30 minutes before LPS injection did not affect LPS-induced hypotension, and the production of NO even increased. Consequently, Cyclosporin’s inability of controlling LPS-induced hypotension is possibly due to its lack of inhibitory properties in NO synthesis. Platonin , a cyanine photosentizing dye, is a cellular photosensitive substance with anti-inflammatory and tissue regeneration effects. Its administration (10 mg/kg) also effectively controls the LPS-induced hypotension, and slows down the generation of NO free radicals. Other than causing hypotension, LPS induces compensatory tachycardia. By giving Minocycline, Clindamycin and Platonin, NO radicals production decreases, the blood pressure climbs up, therefore the heart rate slows down. Since Cyclosporin was unable to control LPS-induced hypotension, tachycardia persists. Although Minocycline, Clindamycin and Platonin were effective in controlling LPS-induced hypotension, survival time did not increase. This might be related to reactive fever caused by hypothalamic LPS stimulation, because these agents could not regulate body temperatures, leading to animal’s hyperthermia and death. Moreover, other biological mediators may have influential effects on decreasing the production of NO radicals. These three drugs have no effects upon other harmful substances despite decreasing the production of NO radicals. Conclusion Minocycline, Clindamycin and Platonin can effectively control LPS-induced hypotension, compensatory tachycardia, by reducing NO radicals production. Cyclosporin though, has no preventive effect against LPS-induced hypotension, due to its lack of ability in slowing down the production of NO radicals. Regardless of whether or not these drugs control LPS-induced hypotension, survival length of laboratory animals showed no improvement. The present experiment offers some parameters for choosing an effective therapeutic agent in the treatment of septicemia, especially in its early stages, in order to prevent the occurrence of complications.
APA, Harvard, Vancouver, ISO, and other styles
6

連國維. "Effects of 2,2,5,7,8-Pentamethyl-6-Hydroxy-Chroman(PMC), A Newly Synthesized NFkB Inhibitor, on Endotoxin- Induced Septic Shock in Rats." Thesis, 1997. http://ndltd.ncl.edu.tw/handle/65132827423801769709.

Full text
Abstract:
碩士
國防醫學院
藥理學研究所
85
It is well established that NO may play an important role in the endotoxin-induced septic shock. 2, 2, 5, 7, 8-pentamethy1-6-hydroxy-chroman (PMC), a newly synthesized NF□B inhibits iNOS gene expression in response to LPS and result in blocking of NO formation in macrophage. The aim of this study was to evaluate the effect of PMC on animal septic shock induced by bolus injection of endotoxin. Results demonstrated that the survival time of PMC-pretreated group was significantly longer than that of untreated control group. The mean arterial pressure was significantly decreased after 4 hours of LPS treatment when compared to control animal. This depressor effect of LPS was markedly reversed by pretreated rats with PMC. Meanwhile, the pressor response to NE in LPS-treated group was significantly attenuated. This hyporeactive effect of NE in LPS-treated group was obviously restored by PMC-treated group. In addition, peak plasma TNF□ & NO levels were markedly increased by LPS-treatment at 1 hr and 4 hr, respectively, during the experimental period. The increase of plasma levels of TNF□ and NO in LPS-treated group was significantly supressed by the pretreatment of rats with PMC. In conclusion, results suggest that PMC may be a clinically potential drug for prevention and treatment of septic shock.
APA, Harvard, Vancouver, ISO, and other styles

Books on the topic "Septic shock; Inhibitors"

1

Wiggers Bernard Conference (6th 1997 Vienna, Austria). Shock, sepsis, and organ failure: Scavenging of nitric oxide and inhibition of its production : sixth Wiggers Bernard Conference, 1997. Berlin: Springer, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Septic Shock: Methods and Protocols (Methods in Molecular Medicine). Humana Press, 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Shock, Sepsis, and Organ Failure: Scavenging of Nitric Oxide and Inhibition of Its Production. Springer, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Septic shock; Inhibitors"

1

Vallance, P., D. Rees, and S. Moncada. "Therapeutic Potential of NOS Inhibitors in Septic Shock." In Nitric Oxide, 385–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57077-3_17.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Fritz, Hans. "Proteinase Inhibitors in Severe Inflammatory Processes (Septic Shock and Experimental Endotoxaemia): Biochemical, Pathophysiological and Therapeutic Aspects." In Ciba Foundation Symposium 75 - Protein Degradation in Health and Disease, 351–79. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720585.ch20.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Martin, Christian, Thierry Roger, and Thierry Calandra. "Macrophage Migration Inhibitory Factor (MIF): A Pro-Inflammatory Mediator of Sepsis." In Evolving Concepts in Sepsis and Septic Shock, 45–67. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1581-4_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Fischer, S. R., and D. L. Traber. "Effects of Nitric Oxide Inhibitors and Hemoglobin in Sepsis." In Shock, Sepsis, and Organ Failure, 273–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-58630-9_13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Hickey, M. J., and P. Kubes. "Nitric Oxide and Leukocyte Adhesion: Experience with NO Inhibitors, NO Donors and iNOS-Deficient Mice." In Shock, Sepsis, and Organ Failure, 163–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-58630-9_8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Whittle, B. J. R., and F. László. "Actions of Selective and Non-selective Nitric Oxide Synthase Inhibitors on Multiple-Organ Microvacular Injury Provoked by Lipopolysaccharide." In Shock, Sepsis, and Organ Failure, 245–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-58630-9_11.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Cuffini, A. M., N. A. Carlone, V. Tullio, and G. Cavallo. "Cell Wall Inhibitors and Bacterial Susceptibility to Phagocytosis." In Host Defense Dysfunction in Trauma, Shock and Sepsis, 979–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77405-8_131.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Gemmell, C. G. "Protein Synthesis Inhibitors and Bacterial Susceptibility to Phagocytosis." In Host Defense Dysfunction in Trauma, Shock and Sepsis, 987–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77405-8_132.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Schlag, Günther, Heinz Redl, H. Gasser, Z. Khakpour, and J. Davies. "Successful Administration of the NO Synthase Inhibitor 546C88 as a Delayed Continuous Infusion in a Baboon Model of Septic Shock." In Shock, Sepsis, and Organ Failure, 23–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-58630-9_2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Green, D. R., R. Marcotte, and N. Wang. "The Role of Inhibitory Cells in Burn Trauma-Associated Immunodeficiency." In Immune Consequences of Trauma, Shock, and Sepsis, 55–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73468-7_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Septic shock; Inhibitors"

1

Martínez-Brotóns, F., J. R. Oncins, J. Mestres, V. Amargós, and C. Reynaldo. "KALLIKREIN-KININ SYSTEM IN PATIENTS WITH SHOCK. COMPARISON BETWEEN SEPTIC AND CARDIOGENIC SHOCK." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644335.

Full text
Abstract:
Alterations of the kallikrein-kinin system (KKS) consistent with activation and increased consumption have been reported in septic patients and it has been suggested that this activation could contribute to the development of septic shock. As similar alterations have been found in other critically ill patients, many of them prone to shock, we wonder if activation of the KKS could be a consequence rather than a cause of the hemodynamic instability. To answer this question we compared 12 patients with septic shock (8 fatal) with 10 cases of cardiogenic shock secondary to myocardial infarction (8 fatal) as a model of non septic shock. In adition 25 episodes of uncomplicated sepsis and 10 intra-intensive care unit controls were studied. A functional measure of factor XII, high molecular weight kininogen (HMWK) (coagulative methods), prekallikrein (PK), Cl-inhibitor (Cl-INH), α2-macroglobulin (α2-M)- Antithrombin III (AT-III) and kallikrein inhibitor activity (KIA) (chromogenic methods) was performedRESULTS: Patients with septic shock, specially in fatal cases, showed a highly significant decrease in activities of factor XII (P<0.001), PK (P<0.0001), HMWK (P<0.005), α2-M (P<0.001), AT-III (P<0.0001) and KIA (P<0.005). Cl-INH activity was increased in uncomplicated sepsis (P<0.001) but came back to normal or was slightly decreased in septic shock. Components and inhibitors of the KKS were within normal limits in all patients with cardiogenic shock.Our findings support the idea of a contribution of the KKS to the development of septic shock but this system neither seems to play a role in the pathogenesis of cardiogenic shock nor to be altered as a consequence of it.
APA, Harvard, Vancouver, ISO, and other styles
2

Egbring, R., R. Seitz, M. Wolf, L. Lerch, and T. Menges. "PROTEINASE-INHIBITOR COMPLEXES (PIC) IN SEPTIC AND NON-SEPTIC SHOCK. COAGULATION; LEUKOCYTE AND BACTERIAL PROTEASE INHIBITION BY MEANS OF PLASMA-INHIBITOR REPLACEMENT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644244.

Full text
Abstract:
In septic or cardiac shock antithrombin III-thrombin (AT III-Thr) and a1antitrypsin-elastase(a1AT-ELP) as well as a2antiplas-min-plasmin (a2AP-Pl) are found to be elevated to different extents. In cardiac shock AT III-Thr is predominantly increased, while in septic disorders a2AT-ELP as indicator of leukocyte stimulation is additionally found to be elevated. Stimuli for leukocyte activation are bacterial endotoxins, immune complexes, factor Xlla and others. The possible action of bacterial proteases during septic infections is only known in animal models. To stop hemorrhagic complications in disseminated intravascular coagulation (DIC) following septic (n=24) or non-septic (n=15) shock, we treated the patients with AT III concentrate and FFP in relatively high amounts containing a2macroglobulin (a2M), a1antitrypsin (a1AT) and others which are not available as concentrates. Subsequent to the procedure PIC's decreased, coagulation factors and inhibitors as well as thrombocyte counts increased. In in vitro models bacterial proteases have been shown to destroy a1AT, activate prothrombin and others. Only a2M may inhibit proteolytic activity of Staph aureus, N. meningitidis, P. aeroginosa and K1. pneumoniae and E. coli as our in vitro studies, using fibrin plates containing a2M, demonstrated. Not only bleeding or microthrombotic complications might be influenced by plasma derivative substitution, but also proteases released from bacteria
APA, Harvard, Vancouver, ISO, and other styles
3

Seitz, R., M. Wolf, R. Egbring, and K. Havemann. "Neutrophil Elastase, Thrombin and Plasmin in Septic Shock: Influence on Prognosis." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643894.

Full text
Abstract:
The prognosis of septicaemia depends on the occurrence of disseminated disturbances of the microcirculation impairing organ function and haemorrhagic complications due to consumption of coagulation factors. The intravasal appearance of three potentially involved proteinases in active form can be detected by immunologic determination of their complexes with inhibitors: thrombin-antithrombin III (TAT), according to PELZER et al. (Thrombos. Haemostas. 54:24,1985); plasmin- antiplasmin (PAP), ldlE, antiserum donated by KARGES; human neutrophil elastase (HNE)- antitrypsin, ELISA, Merck, DarmstadtIn 47 patients with septic shock (19 survived, group A; 28 lethal, group B) the PAP levels were moderately elevated throughout the course without vaviations related to the outcome. TAT was initially strongly increased in both groups (18.8±6.3 ng/ml/16.5±7.2), and decreased towards the end of the course in both groups (2.7±0.5/3.7±0.8). Though the intial HNE levels were higher in group A (2458±348ng/ml) than in group B (1291±295, p=0.017), they decreased, in group A more rapidly and were at the end almost significantly lower than in group B (315±54/652&3x00B1;161, p=0,059). The decrease of TAT as well as HNE was associated with substitution of antithrombin III concentate (ATIII) and fresh frozen plasma (ffp) given with the aim of normalization of haemostasis and replacement of inhibitors. Factor XIII, a substrate of both thrombin and HNE, was initially equally low about 50% of normal in both groups, but increased only in group A (69.1±7.1/49.6±5.5, p=0.045) towards the end.Conclusions: Both TAT and HNE decreased after initial elevation under substitution of ATIII and ffp. A rapid decrease seems to be a favourable sign which is accompanied by rising levels of F XIII, while sustained elevation of HNE points to a poor prognosis
APA, Harvard, Vancouver, ISO, and other styles
4

Qiu, Ping, Xizhong Cui, Junfeng Sun, Judith A. Welsh, Charles Natanson, and Peter Q. Eichacker. "Selective Tumor Necrosis Factor Inhibitors' Effect On Survival In Septic Shock: A Meta-Analysis." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6002.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Xu, Guangtao, Xiaoyan Pan, Guanru Hao, Bijun Shi, Manli Xia, and Xinmei Zhou. "Effect of nitric oxide synthase inhibitors on the changes of hemodynamic parameters and aortic tension induced by septic shock in rats." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6028041.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Schapira, M., B. Waeber, H. R. Brunner, R. Crystal, and M. Courtney. "PROTECTION BY α1-ANTITRYPSIN ALA-357 ARG-358 AGAINST ARTERIAL HYPOTENSION INDUCED BY FACTOR XII FRAGMENT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642801.

Full text
Abstract:
The specificity of serine protease inhibitors belonging to the serpin superfamily depends on the nature of the reactive center amino acid residues. For example, Met→Arg mutation at the reactive center P1 residue (position 358) alters the specificity of α1-antitrypsin (AT) from the Met-specific enzyme neutrophil elastase to the Arg-specific proteases thrombin, plasma kallikrein (K) and activated Factor XII fragment (XIIf). To obtain an inhibitor species which would inhibit K and XIIf but not thrombin, we now have produced by site-directed mutagenesis of cloned AT cDNA an AT variant having Arg at P1 and Ala at P2. This modification at P2 was made because C1-inhibitor, the major inhibitor of K and XIIf, also has Ala at P2. In purified systems, AT Ala-357 Arg-358 inactivated thrombin, K and XIIf with 2nd-order rate constants of 1.1, 21.8 and 0.6 μM-1 min-1 whereas values of 8.5, 4.2 and 2.1 μM-1 min-1 were found with AT Arg-358. Thus, when compared to AT Arg-358, AT Ala-357 Arg-358 was 5.2 times more efficient for inhibiting K but 7.7 times less efficient for inhibiting thrombin. In vivo, AT Ala-357 Arg-358 (0.7 mg i.v.) did not modify the thrombin time of male Wistar rats while a 2-fold prolongation was seen with 0.7 mg AT Arg-358. However, AT Ala-357 Arg-358 (0.7 mg i.v.) partially prevented the kinin-mediated circulatory collapse induced by XIIf (0.1 μg i.v.) since rats (n=4) treated with this double mutant had a blood pressure fall of 14 ±3 (meaniSD) mmHg while control animals (n = 8) receiving saline or AT Val-358 (0.7 mg i.v.) had a decrease of 27 ± 3 mmHg (p<0.01 by t test). AT Ala-357 Arg-358 has therapeutic potential for disease states with activation of the plasma kinin-forming system such as angioedema attacks or septic shock.
APA, Harvard, Vancouver, ISO, and other styles
7

Kodrich, L., P. Porterie, O. Lago, G. Bergonzelli, B. Sassetti, and J. C. Sanchez avalos. "MINI PLASMINOGEN-LIKE MOLECULE IN SEPTIC PATIENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644693.

Full text
Abstract:
We have previously described (Thromb.Res.44(6),1986) an altered relation Plasminogen (Pig)/α2~antiplasmin (APL) (Plg/APL<0.6) in the plasma of septic patients. A probable explanation of the mechanism whereby this alteration takes place would be the degradation of Pig to fragments of lower molecular weight due to the action of leukocyte elastase.In order to confirm this we studied 10 patients with sepsis, which did not have clinicalorlaboratory evidence of disseminated intravascular coagulation or septic shock, with positive blood cultures for bacterial germs .Elastase-α1proteinase inhibitor complexes were measured by an enzyme-linked immunosorbent assay (mean:510±181.9ug/l;normal range:86±28.5ug/l). Pig and APL functional activities were assayed by the amidolytic method; Pig: 40±8.9%; normal range: 100±20% .APL: 95±10.1% formal range 100+20%. Two different behaviors were observed in the plasma Pig of these patients with regard to their capacity to bind to Lysi-ne-Sepharose 4B.0n the basis of this observation the patients were divided into two group.Group A(4 patients) only presented Pig activity in fraction 1 (Pig without lysine binding sites : LBS). Group B (6 patients) presented Pig activity in fraction 1 and in fraction 2 (Pig with LBS).The normal controls presented Pig activity only in fraction 2. All the fractions which presented functional Pig activity also presented immunologic Pig activity and developed areas of lysis in heated fibrin plates after activation with urokinaseIt seems tenable the hypothesis that the action of the leukocyte elastase is responsible for the degradation of Pig and this modification in the molecule would give rise to a greater depuration thus explaining the marked drop of the plasmatic levels seen in septic patients.
APA, Harvard, Vancouver, ISO, and other styles
8

Svartholm, E., U. Haglund, J. Ljungberg, and U. Hedner. "THE EFFECT OF APROTININ ON EXPERIMENTAL PORCINE SEPTIC SHOCK." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644243.

Full text
Abstract:
Septic shock induces pronounced haemodynamic changes resulting in pulmonary microemboliz., complement activ. and an activ. of the coag. and fibrinol. systems. Only minor effects on the sepsis-induced changes were found on pretreatment with a variety of platelet aggr. inhib. (Svartholm et al 1986). Aprotinin inhibits among other enzymes kallikrein. Endotoxin shock was induced in 12 pigs by i .v. inf. of E.coli, six of vdiich got Aprotinin i.v. (1000000 KIE) immediately before the E.coli infusion. Another 6 pigs were used as controls. Haemodynamic parameters, platelet counts, fibrinol. act., fibrinogen, ATIII, and ethanol gel. test were measured before the infusions, 8,60, 90-120, 150-180 min after. Ihe haemodynamic parameters stayed unchanged in the control pigs. In the E. coli-treated animals cardiac output and the mean art. pressure decreased signif. On the other hand, the mean pulm. art. blood pressure and the pulm. vase, resist, increased signif. Ihe increase of the pulm. resist, was less pronounced and reversible in the Aprotinin treated animals. Ihe pulm. vase, resist, in the E.coli group increased contin. from 2.8ଐ.2 mm Hg before to a max. of 23.4 mm Hg at the end of the obs. time and in the Apro-tinin-treated animals from 2.0ଐ.3 to 6.6଑.9 mm Hg (8 min after the inj.) being down to 4.4ଐ.2 at the end of theexp.The platelet decrease was less pronounced in the Aprotinin pretreated group, the ethanol gel test turned pos. in the E.coli group after 60 min but stayed neg. in both the contr. and the Aprotinin pretreated animals. Fibrinolytic act, was seen in all E. coli-treated animals but stayed neg. in the contr. Moderate changes were seen in ATIII and fib. gen in all E.coli-treated pigs. All animals treated with only E.coli died at the end of the obs. time but none in the control group and none in the Aprotinin pretreated groupIn conclusion Aprotinin seems to prevent the secondary fatal increase in pulm. resist, most probably caused by pulm. oedema and a gen. activ. of the coag. syst. (ethanol gel. test stayed neg.)
APA, Harvard, Vancouver, ISO, and other styles
9

Blamback, M., F. Hesselvik, B. Brodin, R. Maller, and R. Gaffney. "COAGUIATION, FIBRINLYSIS AND KALLIKREIN ACTIVATION IN SEVERE INFECTION AND SEPSIS : RELATION TO OUTCOME." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644695.

Full text
Abstract:
Fatal multiple organ failure following severe infection may be related to early activation of protease cascade systems. The study aimed to relate changes in the below mentioned components to shock and outcome. Of 53 patients with severe infection, 30 did not develop shock (group I); 12 survived septic shock (groupII); and 11 died from organ failure after septic shock (groupIII). No patient had overt DIC. During the first 3 days after admission, blood was sampled daily for assay of: platelet count, fibrinogen, prothrombin complex, F XII, F VIIIiC, vWF:Ag, F VII, F V, anti thrombin, protein C, plasminogen, antiplasmin, plasminogen activator inhibitor (PAi), X-oligcmers, D-dimers, prekalli-krein, functional kallikrein inhibition (fKl), and fibronectin, by chramogenic substrate and inmunochemical techniques. The Proenzyme functioned, index (PFI) ves calculated combining the results of anti thrombin, plasminogen, antiplasmin, prekallikrein and fKL (Aasen, Acta Chir Scand 1985; 522: 211).Low (p<.001) initial values for F XII, prothrombin complex, F VII, antithrcmbin, protein C, prekallikrein, and fibronectin were seen in all groups. The shock groups (I-III) had in addition significant decreases in platelet count, antiplasmin, and plasminogen. Fibrinogen, F VIII :C, vWF:Ag, X-oligcmers, and D-dimers were significantly higher than normal in all groups. Shock patients had higher X-oligcmers and D-dimers, but lower fibrinogen than non-shock patients. PAi was within the normal range in survivors (I-II), but was elevated ten-fold and increased progressively over 3 days in the non-survivors. vWF:Ag showed a similar progressive increase in non^survivors; these two variables ware the best early indicators of non-survival. PFI was significantly lower in shock patients (II-III), but did not discern between survivors and non-survivors during days 1-3. The results indicate a marked activation of coagulation in patients with severe infection, with more fibrin formation and fibrinolysis in the shock groups. High vWF:Ag and PAi in non-survivors may indicate nmore endothelial damage, and potentially harmful fibrinolysis inhibition.
APA, Harvard, Vancouver, ISO, and other styles
10

Shashaty, Michael G. S., Nancy E. Kohn, Jason D. Christie, Shiv Kapoor, Mark E. Mikkelsen, Judd E. Hollander, David F. Gaieski, Barry D. Fuchs, Nuala Meyer, and Chirag V. Shah. "Emergency Department Antithrombin III And Plasminogen Activator Inhibitor-1 Initial Plasma Levels Are Associated With Acute Lung Injury In Patients With Severe Sepsis And Septic Shock." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2587.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Septic shock; Inhibitors' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography