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Thèses sur le sujet « Acute Respiratry Distress Syndrome »

Auteur : Grafiati
Publié le 9 mars 2023
Mis à jour le 10 mars 2023

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1

Dushianthan, Ahilanandan. « Phospholipid kinetics in acute respiratory distress syndrome ». Thesis, University of Southampton, 2014. https://eprints.soton.ac.uk/374568/.

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Henderson, William Roy. « Expiratory time constant heterogeneity in experimental acute respiratory distress syndrome ». Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/58370.

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Purpose This thesis evaluated regional heterogeneity of pulmonary mechanical values within models of lung injury. To this end four separate studies were completed. I evaluated regional expiratory time constant (τE) heterogeneity and tissue strain (ε) in a lung model using functional respiratory imaging (FRI) (Study 1, Chapter 2), and developed an in vivo porcine model of lung injury (Study 2, Chapter 3). This model was used to assess changes in τE due to manipulations of respiratory gas density (Study 3, Chapter 4) and mechanical ventilation parameters (Study 4, Chapter 5). Methods Study 1: Using computerized tomography (CT) images we generated 3-dimensional lung models. These were used calculated global and regional values for resistance, elastance, ε and τE under three different airway pressure conditions. Study 2: Experimental lung injury was induced in 11female Yorkshire X pigs. Necropsy, light and electron microscopy of lung was performed. Study 3: I utilized a multi-compartment model to describe the effects of changes in tidal volume (VT) and positive end-expiratory pressure (PEEP) on lung emptying during passive deflation before and after experimental lung injury in 6 adult female Yorkshire X pigs. Expiratory time constants (τE) were determined by partitioning the expiratory flow-volume (V˙ V) curve into multiple discrete segments. Study 4: Tracheal pressure and flow were measured in 7 pigs before and after experimental lung injury. Gas density was altered by using helium-oxygen (He), sulfur hexafluoride-oxygen (SF6) and nitrogen-oxygen (N2) gas. Conclusions Functional respiratory imaging demonstrates regional variation in both ε and τE. These findings raise questions about the use of whole lung measures of ε and τE to guide clinical management of lung injury (Study 1). I developed a stable model of lung injury using SPA that replicates the light and electron microscopic findings seen in human ARDS (Study 2). A pragmatic strategy using changes in the pattern of expiration described by a multi-compartment model of τE reveals that alterations in and gas density (Study 3) as well as PEEP and VT (Study 4) change expiratory pulmonary mechanics. These observations lay the groundwork for future clinical studies in lung injured patients.
Education, Faculty of
Kinesiology, School of
Graduate
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3

Camprubí, Rimblas Marta. « Nebulized anti-coagulants as a therapy for acute lung injury and acute respiratory distress syndrome ». Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/663961.

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La síndrome de distrés respiratori agut (ARDS) és una insuficiència respiratòria aguda amb una incidència global a Europa de 17,9 per cada 100.000 persones-any. Tot i els avenços en el tractament de suport dels pacients amb ARDS, la mortalitat continua sent alta (40%) i els pacients que sobreviuen presenten seqüeles persistents. Actualment no existeix un tractament efectiu. La fisiopatologia de l’ARDS es caracteritza per l’activació de la coagulació i la inflamació a nivell pulmonar, juntament amb el trencament de la barrera alveolar-capil·lar. Això comporta la formació d’edema proteic, la infiltració dels neutròfils cap al compartiment alveolar i l'activació dels macròfags cap a un fenotip pro-inflamatori. Estudis previs en models pre-clínics de lesió pulmonar aguda (ALI) i en pacients amb ARDS han demostrat els efectes beneficiosos del anti-coagulants, tot i que aquests efectes positius es veuen contrarestats pel risc d’hemorràgia sistèmica. Els anti-coagulants podrien ser efectius gràcies a la seva activitat anti-inflamatòria a més de les seves propietats anti-coagulants. Atesa l’estreta interacció entre aquestes vies i la seva influència en la permeabilitat, els anti-coagulants també podrien restaurar la barrera alveolar-capil·lar. La nebulització dels anti-coagulants directament al compartiment alveolar podria augmentar l'eficàcia local i disminuir el risc d'hemorràgia sistèmica. La hipòtesi d'aquesta tesi és que l'heparina nebulitzada i/o antitrombina (ATIII) limitaran la resposta pro-inflamatòria i pro-coagulant pulmonar després de la LPA, promovent, també, la restauració de la barrera alveolar-capil·lar. La co-administració dels anti-coagulants directament als pulmons mitjançant nebulització produirà un efecte sinèrgic que potenciarà les propietats de l'heparina i l’ATIII, reduint la lesió pulmonar i evitant el risc d'hemorràgia sistèmica. Com a part d’aquesta tesi es mostren els resultats de l'acció de l'heparina o l’ATIII específicament en poblacions pulmonars primàries de cèl·lules humanes lesionades i l'administració directa d'heparina i/o ATIII als pulmons per nebulització en un model de rata d’ALI. La nebulització d'heparina i/o d’ATIII atenuen la inflamació i coagulació pulmonar sense produir hemorràgia sistèmica en el model d’ALI. El tractament amb heparina nebulitzada modula els macròfags alveolars mitjançant la reducció dels efectors de TGF-β i NF-κB i la via de coagulació i disminueix el reclutament de neutròfils a l'espai alveolar. L'administració local d'ATIII augmenta els efectes beneficiosos en la coagulació, mentre que la combinació d'ATIII i heparina tenen un major impacte en la reducció de la permeabilitat i la disminució de la infiltració de macròfags en el compartiment alveolar. En estudiar l'acció translacional en humans d'ambdós anti-coagulants en poblacions cel·lulars humanes lesionades aïllades de biòpsies pulmonars, l'heparina disminueix l'expressió de marcadors proinflamatoris en els macròfags alveolars i desactiva la via NF-κB en cèl·lules alveolars tipus II; disminuint l'expressió dels seus mediadors i efectors. D’altra banda, l'ATIII redueix els nivells de mediadors proinflamatoris i augmenta les unions estretes en les cèl·lules alveolars tipus II lesionades. Els estudis actuals demostren que l'heparina nebulitzada i l'ATIII poden ser un tractament potencial per a la ARDS, ja que actuen en diferents vies i processos de la fisiopatologia d’aquesta síndrome. L'administració local d'anti-coagulants atenua la lesió pulmonar disminuint la inflamació, la coagulació i proveeix millores en la permeabilitat sense causar hemorràgia sistèmica.
Acute respiratory distress syndrome (ARDS) is an acute respiratory failure with a global incidence in Europe of 17.9 per 100,000 person-year. Although significant advances have been performed in supportive care of patients with ARDS, mortality remains high (40%) and survivors present persistent sequelae. An effective pharmacological therapy for this syndrome is not available yet. ARDS pathophysiology involves pulmonary activated coagulation and inflammation together with the breakdown of the alveolar-capillary barrier. This leads to proteinaceous edema, neutrophils infiltration into the alveolar compartment and the activation of macrophages towards a pro-inflammatory phenotype. Beneficial effects of anti-coagulants have been proved in pre-clinical models of acute lung injury (ALI) and in ARDS patients, although systemic bleeding offset its positive effects. Anti-coagulants could be effective for their anti-inflammatory activity in addition to their anti-coagulant properties. Moreover, given the cross talk of these pathways and their influence on permeability, anti-coagulants could also restore the alveolar-capillary barrier. Nebulization of anti-coagulants directly into the alveolar compartment might increase local efficacy and decrease the risk of systemic bleeding. The hypothesis of this thesis is that nebulized heparin and/or antithrombin (ATIII) limit the pro-inflammatory and pro-coagulant response in the lungs after ALI, also promoting the restoration of the alveolar-capillary barrier. The co-administration of both anti-coagulants directly into the lungs via nebulization produces a synergistic effect enhancing the properties of heparin and ATIII, reducing lung injury and avoiding the risk of systemic bleeding. As part of this thesis we are showing the results of the action of heparin or ATIII in specific primary human injured cell lung populations and the direct administration of heparin and/or ATIII into the lungs by nebulization in a rat model of ALI. Nebulized heparin and/or ATIII attenuated pulmonary inflammation and coagulation and did not produce systemic bleeding in the model of ALI. Treatment with nebulized heparin modulated alveolar macrophages through reducing TGF-β and NF-κB effectors and the coagulation pathway and decreased the recruitment of neutrophils into the alveolar space. Local administration of ATIII alone increased beneficial effects in coagulation, while combined ATIII and heparin had a higher impact reducing permeability and decreasing the infiltration of macrophages into the alveolar compartment. The translational action into humans of both anti-coagulants was also studied. In injured human cell lung populations isolated from lung biopsies, heparin diminished the expression of pro-inflammatory markers in alveolar macrophages and deactivated the NF-κB pathway in alveolar type II cells; decreasing the expression of its mediators and effectors. Also, ATIII decreased levels of pro-inflammatory mediators and increased levels of tight junctions in injured alveolar type II cells. The current studies prove that nebulized heparin and ATIII might be a potential treatment for ARDS, as they act in different pathways and processes of the pathophysiology of this syndrome. Local administration of anti-coagulants attenuates lung injury decreasing inflammation, coagulation and proving ameliorations on permeability without causing systemic bleeding.
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4

Peters, Mark John. « The role of platelets in acute inflammation ». Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271069.

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5

Greene, Michelle Kathleen. « Therapeutic evaluation of an immunomodulatory nanoparticle in acute respiratory distress syndrome ». Thesis, Queen's University Belfast, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.680123.

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Acute Respiratory Distress Syndrome (ARDS) is characterised by dysregulated inflammation within the lungs, which can severely compromise pulmonary architecture and function. Despite intensive efforts to develop therapies for ARDS, there are no curative pharmacological interventions at present. Instead, management of ARDS is primarily supportive and the syndrome is associated with substantial mortality, morbidity and healthcare expenditure. In pursuit of an effective ARDS therapy, this thesis explored the potential application of a novel sialic acid-functionalised nanoparticle (SNP). This nanoplatform was designed to actively target sialic acid-binding immunoglobulin-like lectin (Siglec) receptors expressed on monocytes and macrophages, which exert a fundamental role in the negative regulation of inflammatory responses. Initially, SNP were evaluated in a murine model of lipopolysaccharide (LPS)-induced lung injury, where promising outcomes were observed. SNP attenuated several lung injury parameters in this model, including neutrophilia and pro-inflammatory cytokine levels in the pronchoalveolar lavage fluid (BALF), amongst others. Crucially, the translational efficacy of SNP was confirmed in human models of LPS-induced inflammation. SNP inhibited pro-inflammatory cytokine production in cultures of primary human cells implicated in ARDS, whilst concurrently enhancing levels of antiinflammatory interleukin (IL)-10. The protective effects of SNP were also evident in whole human lungs injured with LPS ex vivo, where reductions in pulmonary oedema and BALF cellularity were observed. Collectively, these findings highlight the potential of SNP to combat the inflammatory component of ARDS and fulfill the clinical need for an effective therapy.
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Singh, Nanak. « Incidence and pathogenesis of acute lung injury and the acute respiratory distress syndrome in humans ». Thesis, University of East Anglia, 2013. https://ueaeprints.uea.ac.uk/48050/.

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Acute lung injury (ALI) and it’s more severe form, acute respiratory distress syndrome (ARDS), are conditions characterised by neutrophilic pulmonary inflammation, refractory hypoxaemia and diffuse alveolar damage. This work reports on the first UK based prospective study of the incidence and longer term mortality of ALI/ARDS in a general intensive care unit. Results reveal significant under recognition of this condition, which occurred in 12.5% of the ICU population (n=344). Hospital and 2 year mortality rates were 50-55% and 58-61% respectively. Neutrophils are central in the pathogenesis of ALI/ARDS. Neutrophil priming, a reversible process whereby the response of neutrophils to an activating stimulus is up-regulated by prior exposure to a priming agent, is a pre-requisite for neutrophil-mediated tissue damage. Comparisons of the trans-pulmonary gradient of several markers of neutrophil priming were made in different patient groups. Patients with sepsis but healthy lungs (n=6) were found to have a positive trans-pulmonary gradient with respect to neutrophil expression of CD62L, suggesting that CD62L ‘low’ (primed) neutrophils are being de-primed in the pulmonary circulation. In patients with ARDS this gradient was reversed, suggesting that neutrophils are being primed within the lung. This leads to the novel hypothesis that, in conditions such as sepsis, neutrophils primed systemically may be held in the pulmonary capillary bed and there allowed to de-prime, before being released in a quiescent state. Failure of this process may allow net accumulation of primed neutrophils in the lung with consequent lung injury. Currently there are no effective pharmacological therapies for ALI/ARDS, which is compounded by the relative lack of human models. An 18 month, prospective study of the incidence of ALI/ARDS post oesophagectomy revealed an incidence of 31% and suggested intra-operative one lung ventilation as a causative factor. Hence, patients undergoing oesophagectomy present an attractive model for future ALI/ARDS research.
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7

Quinlan, Gregory John. « Oxidative damage to extracellular proteins and lipids during acute lung injury ». Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281713.

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8

Aggarwal, Anjna. « Mediators and mechanisms of persistent pulmonary neutrophilia in acute lung injury ». Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289880.

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9

Jordan, Simon James. « The pathogenesis of lung injury following cardiothoracic surgery ». Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249727.

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10

Crag, Thelma R. « Investigation into the mechanisms and treatment of acute living injury and the acute respiratory distress syndrome ». Thesis, Queen's University Belfast, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534709.

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11

Rocksʹen, David. « Acute lung injury : study of pathogenesis and therapeutic interventions / ». Umeå : Univ, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-161.

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12

Baker, Cathy Sue. « Rationale for surfactant replacement therapy in patients with acute lung injury ». Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243281.

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13

Jia, Xiaoming M. Eng Massachusetts Institute of Technology. « The effects of mechanical ventilation on the development of Acute Respiratory Distress Syndrome ». Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/41629.

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Thesis (M. Eng.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2007.
Includes bibliographical references (p. 74-76).
Acute Respiratory Distress Syndrome (ARDS) is a severe lung illness characterized by inflammation and fluid accumulation in the respiratory system. Historically, ARDS and other forms of respiratory failure have been treated using mechanical ventilation to help maintain gas exchange in the lungs. However, clinical investigators are beginning to discover the adverse effects of mechanical ventilation if it is not applied properly. Specifically, excessive ventilator volumes and pressures may exacerbate existing lung injury and increase hospital mortality. Furthermore, aggressive ventilation may cause lung injury and trigger an inflammatory response that is characteristic of ARDS. These findings have alarmed the critical care community, and many studies have been conducted to find mechanical ventilator settings that reduce mortality in patients with ARDS. However, there have been no firm recommendations on the optimal settings for patients who require ventilator therapy for reasons apart from respiratory failure. In this thesis, we retrospectively examine a large medical database (MIMIC-II) to study the relationship between mechanical ventilation and the development of ARDS. Specifically, our goals are to (1) find patients who did not have ARDS at the beginning of mechanical ventilation but who later developed the disease; (2) identify physiologic and ventilator-associated risk factors for ARDS; and (3) develop a text analysis algorithm to automatically extract clinical findings from radiology (chest x-ray) reports. Our findings suggest that acute respiratory distress syndrome is a relatively common illness in patients who require mechanical ventilation in the ICU (152 of 789 without ARDS at the outset eventually developed the disease).
(cont.) High plateau pressure (odds ratio 1.5 per 6.3 cmH20, p < 0.001) is the most important ventilator-associated risk factor for the development of new ARDS. Physiologic risk factors include high weight, low blood pH, high lactate, pneumonia, and sepsis. Thus it may be possible to reduce the occurrence of ventilator-induced lung injuries with careful pressure management. However, a randomized prospective study is needed to support this hypothesis.
by Xiaoming Jia.
M.Eng.
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BELLANI, GIACOMO. « Imaging of lung metabolic activity by means of positron emission tomography during acute lung injury ». Doctoral thesis, Università degli Studi di Milano-Bicocca, 2010. http://hdl.handle.net/10281/7887.

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Neutrophilic inflammation plays a key role in the pathogenesis of acute respiratory distress syndrome (ARDS) and acute lung injury (ALI). Positron emission tomography (PET) with [F]-fluoro-2-deoxy-D-glucose (FDG) can be used to image cellular metabolism that, during lung inflammatory processes, likely reflects neutrophils activity. The aim of this study was to assess the magnitude and regional distribution of inflammatory metabolic activity in the lungs of patients with ALI/ARDS by PET with FDG. Fifteen patients with ALI/ARDS were enrolled, while four spontaneously breathing and two mechanically ventilated subjects, without known lung disease, served as controls. In each individual we performed an FDG PET/computed tomography of the thorax. FDG cellular influx rate constant (Ki) was computed for the imaged lung field and for regions of interest, grouping voxels with similar density. In all patients with ALI/ARDS, Ki was higher than in controls, also after accounting for the increased lung density. Ki values differed greatly among patients, but in all patients Ki of the normally aerated regions was much higher (2- to 24-fold) than in controls. Whereas in some patients the highest Ki values corresponded to regions with the lowest aeration, in others these regions had lower Ki than normally and mildly hypoaerated regions. In patients with ALI/ARDS, undergoing mechanical ventilation since days, the metabolic activity of the lungs is markedly increased across the entire lung density spectrum. The intensity of this activation and its regional distribution, however, vary widely within and between patients.
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Morrison, Thomas. « Human mesenchymal stromal cell regulation of pulmonary macrophage populations in the Acute Respiratory Distress Syndrome ». Thesis, Queen's University Belfast, 2017. https://pure.qub.ac.uk/portal/en/theses/human-mesenchymal-stromal-cell-regulation-of-pulmonary-macrophage-populations-in-the-acute-respiratory-distress-syndrome(da547b07-7974-436a-8943-7e2ddf3933cc).html.

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The Acute Respiratory Distress Syndrome (ARDS) is a devastating clinical disorder characterised by excessive inflammation in the alveolar compartment resulting in oedema of the airspaces due to loss of integrity in the alveolar epithelial-endothelial barrier. ARDS is associated with high mortality rates and there are currently no effective pharmacological therapies available. Human Mesenchymal Stromal Cells (hMSCs) are a promising candidate therapy which are currently being investigated in clinical trials for ARDS. However their mechanisms of effects in lung injury are not fully elucidated. A fuller understanding of these mechanisms may highlight novel therapeutic targets, identify potency assays to inform hMSC donor selection or biomarkers to assess their efficacy in clinical samples. The alveolar macrophage (AM) is key to orchestrating the inflammatory response in lung injury highlighting the AM as an ideal therapeutic target. hMSCs are known for their immunomodulatory capacity and so it was hypothesised that hMSCs could modulate human macrophage function to adopt a more anti-inflammatory phenotype. The aims of this project were to investigate the effect of hMSCs on human macrophage phenotype and function and to determine the mechanisms of these effects. hMSCs were able to promote an anti-inflammatory (M2-like) macrophage phenotype in lipopolysaccharide or ARDS patient bronchoalveolar lavage fluid-treated human macrophages. This phenotype was characterised by a dampened inflammatory cytokine secretory profile, increased expression of the classical M2 macrophage marker CD206 and enhanced phagocytic capacity. Blocking hMSC-derived extracellular vesicle (EV) uptake by human macrophages using anti-CD44 antibody reversed these effects. Moreover, the adoptive transfer of murine AMs which had been pre-treated with hMSC-derived EVs was protective in endotoxin-induced lung injury in vivo highlighting the AM as a key cellular mediator of hMSC beneficial effects. A proportion of hMSC-EVs were found to contain mitochondria which were transferred to human macrophages in vitro facilitating hMSCs modulatory effects through the enhancement of macrophage mitochondrial oxidative phosphorylation. These data report a novel mechanism by which hMSCs modulate macrophage phenotype in in vitro and in vivo models of ARDS.
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Chen, Yan Mi. « Regulation of iron mediated signalling processes during endotoxaemia : implications for the acute respiratory distress syndrome ». Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395766.

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Martin, Collin Armand. « Pathology of complicated Babesia rossi-associated acute lung injury and respiratory distress syndrome in dogs ». Diss., University of Pretoria, 2020. http://hdl.handle.net/2263/77412.

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A proportion of Babesia rossi infections in dogs are classified as complicated. One of the most lethal complications is the acute lung injury (ALI) and acute respiratory destress syndrome (ARDS). Patients affected by this complication usually succumb within 24 hours and there are similarities between this disease and malaria associated ALI and ARDS in humans, both rapidly fatal conditions. Both diseases are caused by haemoprotozoal parasites transmitted by insect vectors, namely ticks for babesiosis and mosquitoes for malaria. The pulmonary pathology of complicated babesiosis is poorly described and the aim of this study is to provide a thorough histomorphological analysis with immunohistochemical labelling of leukocytes to further define the immune cell population. The left caudal lung lobes from 11 Babesia rossi infected dogs and 4 healthy controls were examined with standard light microscopy and immunohistochemical markers applied. Markers included CD204 (resident tissue macrophages and dendritic cells), MAC387 (monocyte-macrophages of bone marrow origin), CD3 (mature T-lymphocytes), CD20 (mature B-lymphocytes and normal plasma cells), Mum-1 (plasma cells) and PAX-5 (immature and mature B-lymphocytes). Histopathology showed a severe increase in monocyte-macrophages within the alveolar walls and lumens. This was invariably accompanied by alveolar oedema as well as multifocal to coalescing areas of haemorrhage. Immunohistochemical labelling showed a significant increase in MAC387, CD204 and CD3 positive cells in the infected cases compared to healthy control dogs. This study provided novel insights into the pathology of and similarities between babesia and malaria associated ALI/ARDS in dogs and humans, respectively. Further fine ultrastructural examination of the pulmonary vascular endothelium is required in future studies.
Dissertation (MMedVet (Pathology))--University of Pretoria, 2019.
Paraclinical Sciences
MMedVet (Pathology)
Unrestricted
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Güldner, Andreas, Robert Huhle, Alessandro Beda, Thomas Kiss, Thomas Bluth, Ines Rentzsch, Sarah Kerber et al. « Periodic Fluctuation of Tidal Volumes Further Improves Variable Ventilation in Experimental Acute Respiratory Distress Syndrome ». Frontiers Research Foundation, 2018. https://tud.qucosa.de/id/qucosa%3A32492.

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In experimental acute respiratory distress syndrome (ARDS), random variation of tidal volumes (VT ) during volume controlled ventilation improves gas exchange and respiratory system mechanics (so-called stochastic resonance hypothesis). It is unknown whether those positive effects may be further enhanced by periodic VT fluctuation at distinct frequencies, also known as deterministic frequency resonance.We hypothesized that the positive effects of variable ventilation on lung functionmay be further amplified by periodic VT fluctuation at specific frequencies. In anesthetized and mechanically ventilated pigs, severe ARDS was induced by saline lung lavage and injurious VT (double-hit model). Animals were then randomly assigned to 6 h of protective ventilation with one of four VT patterns: (1) random variation of VT (WN); (2) P04, main VT frequency of 0.13Hz; (3) P10, main VT frequency of 0.05Hz; (4) VCV, conventional non-variable volume controlled ventilation. In groups with variable VT , the coefficient of variation was identical (30%). We assessed lung mechanics and gas exchange, and determined lung histology and inflammation. Compared to VCV, WN, P04, and P10 resulted in lower respiratory system elastance (63 ± 13 cm H2O/L vs. 50 ± 14 cm H2O/L, 48.4 ± 21 cm H2O/L, and 45.1 ± 5.9 cm H2O/L respectively, P < 0.05 all), but only P10 improved PaO2/FIO2 after 6 h of ventilation (318 ± 96 vs. 445 ± 110mm Hg, P < 0.05). Cycle-by-cycle analysis of lung mechanics suggested intertidal recruitment/de-recruitment in P10. Lung histologic damage and inflammation did not differ among groups. In this experimental model of severe ARDS, periodic VT fluctuation at a frequency of 0.05Hz improved oxygenation during variable ventilation, suggesting that deterministic resonance adds further benefit to variable ventilation.
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Dancer, Rachel Catherine Anne. « Investigation into a potential role for vitamin D in the pathogenesis of acute respiratory distress syndrome ». Thesis, University of Birmingham, 2017. http://etheses.bham.ac.uk//id/eprint/7859/.

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Patients undergoing oesophagectomy are at risk of developing Acute Respiratory Distress Syndrome (ARDS), an immune mediated form of severe respiratory failure. The immunomodulatory properties of Vitamin D are increasingly recognised. We hypothesised that preoperative Vitamin D supplementation would reduce levels of perioperative alveolar oedema in patients undergoing oesophagectomy. Vitamin D deficiency is common in patients with and at risk of ARDS. High dose supplementation with cholecalciferol is a safe and effective method of increasing Vitamin D levels. Supplementation reduces perioperative increases in inflammatory alveolar oedema. Circulating levels of the active form of Vitamin D relate to long term post-operative mortality. Patients who survive at least 2 years post-op have higher preoperative circulating numbers of Natural Killer cells. We did not find any evidence of an effect of Vitamin D on Natural Killer Cells. In conclusion, preoperative Vitamin D status relates to perioperative changes in inflammatory alveolar oedema and high dose Vitamin D supplementation is a safe and effective method of improving preoperative Vitamin D status. Preoperative cholecalciferol administration should be considered in patients with and at risk of vitamin D deficiency.
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Hamid, Umar Imran. « Use of clinically relevant human models to test novel therapies for the acute respiratory distress syndrome ». Thesis, Queen's University Belfast, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.695362.

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In the current era, there are no effective therapies for the treatment of acute respiratory distress syndrome (ARDS) despite numerous clinical trials. Current strategies are aimed at improving pulmonary perfusion, recruitment of atelectatic alveoli and reducing iatrogenic injuries to the lung. The human models of ARDS give important information when testing potential drug therapies and serve as a bridge between experimental studies and phase 11/111 clinical trials. I was able to establish the ex vivo lung perfusion model and studied the effects of aspirin in reducing pulmonary inflammation produced by lipopolysaccharide (LPS). To translate the beneficial effect of aspirin on pulmonary inflammation seen in experimental models of ARDS into a phase I clinical trial, the healthy volunteer model of LPS inhalation was used. Aspirin in these human models of ARDS was shown to reduce the pulmonary makers of inflammation due to its anti-inflammatory properties, however further clinical studies will be required to establish its role as a potential drug therapy for ARDS.
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Sales, Raquel Pinto. « Acute Respiratory Distress Syndrome (ARDS) is an inflammatory disease characterized by pulmonary edema, stiff lungs and hypoxemia ». Universidade Federal do CearÃ, 2014. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=12672.

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Acute Respiratory Distress Syndrome (ARDS) is an inflammatory disease characterized by pulmonary edema, stiff lungs and hypoxemia. Patients with ARDS are more susceptible to VILI (ventilator induced lung injury). Under mechanical ventilation, lung stress and strain are the main determinants of VILI and in patients with muscle effort patient-ventilator asynchrony may enhance this phenomenon. Ventilation modes PCV and VCV with auto-flow can minimize patient-ventilator asynchrony, but then can liberate the offer of flow and tidal volume, compromising the protective ventilatory strategy in ARDS. This study aimed to evaluate the influence of muscle effort and patient-ventilator asynchrony on pulmonary stress and strain in a mechanic lung model of acute respiratory distress syndrome. An experimental bench study was performed, using a lung simulator, ASL 5000TM, in which was configured a lung model with restrictive respiratory mechanics with complacency of 25ml/cmH2O and resistance of 10 cmH2O/L/sec. Muscle effort was adjusted in three situations: no muscular effort (Pmus = 0), with inspiratory muscle effort (Pmus = -5 cmH2O) and inspiratory and expiratory effort (Pmus = -5/+5 cmH2O), all with breathe rate (b) of 20 bpm. Five ventilators were connected to the simulator through and endotracheal tube No 8.0 mm and adjusted on VCV, VCV with Auto-flowTM (in the ventilator in which it was available) and PCV modes, all with tidal volume (VT): 420 ml, PEEP: 10 cmH2O and breath rate set in two situations: b = 15 bpm (lower than b of the respiratory muscle effort) and b = 25 bpm (higher than b of the respiratory muscle effort). Variables analyzed were: maximum VT, alveolar pressure at the end of inspiration, effective PEEP, driving pressure, transpulmonary pressure at the end of inspiration and expiration, average transpulmonary pressure, inspiratory peak flow and analysis of mechanic curves. In the studied lung model the b of the ventilator adjusted higher of the b of the patient and not the muscle effort was the main determinant for the development of patient-ventilator asynchrony, causing large variations of the VT and pulmonary pressures, intensifying the lung stress and strain. The ventilatory modes had similar behavior, although VCV Auto-flowTM and PCV have presented slightly higher values of VT and pulmonary pressures. Thus it is concluded that the proper adjustment of the programed breath rate in the assisted/controlled modes can minimize patient-ventilator asynchrony, reducing lung stress and strain.
A SÃndrome da AngÃstia RespiratÃria Aguda (SARA) à uma doenÃa inflamatÃria caracterizada por edema pulmonar, pulmÃes rÃgidos e hipoxemia. Pacientes com SARA estÃo mais suscetÃveis à VILI (ventilator induced lung injury). Sob ventilaÃÃo mecÃnica, o stress e o strain pulmonares sÃo os principais determinantes da VILI e nos pacientes com esforÃo muscular a assincronia paciente-ventilador pode potencializar este fenÃmeno. Os modos ventilatÃrios PCV e VCV com AutoFlow podem minimizar a assincronia paciente-ventilador, mas por outro lado podem liberar a oferta de fluxo e volume corrente, comprometendo a estratÃgia ventilatÃria protetora na SARA. Objetivou-se avaliar as influÃncias do esforÃo muscular e da assincronia paciente-ventilador sobre o âstrainâ e o âstressâ pulmonares em modelo pulmonar mecÃnico de sÃndrome da angÃstia respiratÃria aguda. Foi realizado um estudo experimental de bancada, utilizando um simulador de pulmÃo, ASL 5000 no qual foi configurado um modelo pulmonar com mecÃnica respiratÃria restritiva, com complacÃncia de 25ml/cmH2O e resistÃncia de 10 cmH2O/L/sec. O esforÃo muscular foi ajustado em trÃs situaÃÃes: sem esforÃo muscular (Pmus=0), com esforÃo muscular inspiratÃrio (Pmus= -5cmH2O) e esforÃo inspiratÃrio e expiratÃrio (Pmus= -5/+5 cmH2O), todos com frequÃncia respiratÃria (f) de 20rpm. Ao simulador foram conectados cinco ventiladores atravÃs de um tubo orotraqueal n 8,0 mm e ajustados nos modos VCV, VCV com sistema AutoFlow (no ventilador que tinha o sistema disponÃvel) e PCV, todos com volume corrente (VC): 420 ml, PEEP: 10 cmH2O e frequÃncia respiratÃria programada em duas situaÃÃes: f=15rpm (< que a f de esforÃo muscular respiratÃrio) e f=25rpm (> que a f de esforÃo muscular respiratÃrio). As variÃveis analisadas foram: VC mÃximo, a pressÃo alveolar no final da inspiraÃÃo, PEEP efetiva, driving pressure, pressÃo transpulmonar no final da inspiraÃÃo e expiraÃÃo, pressÃo transpulmonar mÃdia, pico de fluxo inspiratÃrio e anÃlise das curvas de mecÃnica. No modelo pulmonar estudado a f do ventilador pulmonar ajustada acima da f do paciente e nÃo o esforÃo muscular o principal determinante para o desenvolvimento de assincronia paciente ventilador, causando grandes variaÃÃes de VC e pressÃes pulmonares, o que intensificou o stress e strain pulmonares. Os modos ventilatÃrios tiveram comportamento semelhante, embora os modos VCV AutoFlow e PCV tenham apresentado valores discretamente maiores de VC e pressÃes pulmonares. Desta forma conclui-se que o ajuste adequado da frequÃncia programada nos modos assistido/controlado podem pode minimizar a assincronia paciente ventilador reduzindo o stress e strain pulmonares. Palavras-
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Medford, Andrew R. L. « The role of vascular endothelial growth factor (VEGF) in repair and recovery from acute respiratory distress syndrome (ARDS) ». Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/6661.

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Acute Respiratory Distress Syndrome (ARDS) is the most extreme form of acute lung injury and continues to have a significant morbidity and mortality. Unfortunately, the mechanisms involved in the recovery and repair of the lung following ARDS remain poorly understood. An understanding of these is pivotal to improving outcome from acute lung injury. Several observational studies have suggested a potential relationship between Vascular Endothelial Growth Factor (VEGF) in the lung and the development/outcome of ARDS. In this thesis, three potential mechanisms underlying these observations have been explored: 1. What is the anatomical distribution of VEGF receptor and isoform expression in normal and ARDS lung? How does this change at early and later time points following acute lung injury? 2. Are human type 2 alveolar epithelial (ATII) cells a source of and target for VEGF? How does exposure to a pro-inflammatory milieu modify their expression of VEGF isoforms and receptors? 3. Is there a relationship between a functional VEGF polymorphism and susceptibility to developing and severity of ARDS? I have demonstrated VEGF receptor expression on both sides of the alveolarcapillary membrane with upregulation in later ARDS. All three principal isoforms (VEGF121, VEGF165 and VEGF189) are expressed in normal human lung with uniform downregulation of all three in early ARDS, which normalises with increasing time following injury. I have not found any evidence of VEGF isoform switching. I have also demonstrated human ATII cells are both a significant cellular source of and a target for VEGF (via VEGF receptor expression) confirming autocrine VEGF activity in the lung. VEGF is an ATII cell survival factor. ATII cells differentially respond to pro-inflammatory stimuli by increasing VEGF isoform but not receptor expression, which may serve as a regulatory control mechanism. Finally, I have demonstrated the VEGF 936 T allele increases susceptibility to and the severity of lung injury. The T allele is associated with an increase in plasma VEGF level in ARDS patients but intra-alveolar levels are unaffected.
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23

Tubau, Llopart Isabel. « Biomarkers of oxidative stress in acute respiratory distress syndrome in exhaled breath measured online by mass spectrometry ». Doctoral thesis, Universitat Autònoma de Barcelona, 2012. http://hdl.handle.net/10803/96305.

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Introducció: En el context de la síndrome del destret respiratori agut (SDRA), neutròfils activats emigren dels capil·lars pulmonars cap a l’alvèol i a l'espai intersticial, on alliberen radicals lliures d'oxigen anomenats espècies reactives de l’oxigen (ROS) que juguen un paper molt important en la patogènesis del SDRA. La secreció de ROS i d'altres mediadors proinflamatoris culminen en la lesió de la membrana alveolo-capil·lar, causant increment de la permeabilitat i edema pulmonar. Quan ROS interaccionen amb els lípids de les membranes de les cèl·lules pulmonars, té lloc un procés anomenat peroxidació lipídica, que dóna lloc, en última instància, a la generació de components orgànics volàtils (VOCs) com pentà, malondialdehid, propionaldehid i acetona. Donat que aquests components són volàtils i s’originen primerament en el pulmó, s’esperaria que fossin trobats en l’aire exhalat abans que en la sang. Objectius: L'objectiu principal fou determinar si els prèviament esmentats productes de peroxidació lipídica poden ser mesurats on-line en l'aire expirat dels pacients amb SDRA i si la seva concentració és més alta en comparació amb el grup control, sense lesió pulmonar aguda. Els objectius secundaris foren determinar: i) la resposta inflamatòria sistèmica a través de la proteïna C-reactiva, interleuquina-6 i procalcitonina en sang; ii) si hi ha associació lineal entre les concentracions dels diferents VOCs i entre els VOCs i els marcadors d'inflamació sistèmics, així com també entre VOCs i severitat de la lesió pulmonar expressada per l’escala LIS (Lung Injury Score) i PaO2/FiO2. Disseny: Anàlisi transversal dels VOCs i dels marcadors d’inflamació sistèmics dins d'un estudi observacional prospectiu descriptiu de paràmetres clínics portat a terme en el període 2009-2011. Context: Unitat de Cures Intensives medicoquirúrgica en un hospital universitari amb 20 llits. Pacients: Es van incloure de manera prospectiva pacients amb SDRA (dins de les primeres 48h del diagnòstic) (n=16) i pacients ventilats mecànicament sense lesió pulmonar aguda i sense infiltrats alveolars en la radiografia de tòrax (n=14), durant qualsevol moment del seu ingrés. Els pacients amb SDRA van ser ventilats segons les recomanacions de la ARDS-Network. Es van enregistrar paràmetres demogràfics, fisiològics, clínics, radiològics i bioquímics. Es van utilitzar les escales SAPS II (Simplified Acute Physiological Score) i el LIS per avaluar la severitat de la malaltia en el moment de la mesura de l'aire exhalat . L’aplicació d’assistència pulmonar extracorpòria (oxigenació per membrana extracorpòria (ECMO) o l’assistència pulmonar extracorpòria sense bomba (iLA)) va ser considerada en pacients amb SDRA que no van respondre al tractament estàndard optimitzat. Intervenció: La baixa concentració de VOCs en l'aire expirat requereix un mètode supersensible per detectar-los. Amb aquesta finalitat es va utilitzar l’espectrometria de masses reacció ió/molècula (IMR-MS). Aquesta tècnica permet la mesura no invasiva i en temps real de la mostra. Mostres d'aire alveolar obtingudes mitjançant l'accionador del llindar de CO2 van ser analitzades connectant els pacients al IMR-MS, a través d'una peça en T situada entre el tub endotraqueal i el connector en Y del respirador. Mostres de l’aire inspirat van ser obtingudes a través d’una peça en T col·locada directament en el circuit del respirador. Paràmetres biològics i bioquímics van ser analitzats en el moment de la mesura de l’aire exhalat. Resultats principals: No es van trobar diferències en relació a l’edat, sexe, índex de massa corpòria o comorbiditats entre els dos grups. Com era d’esperar, les puntuacions en les escales de SAPS II i LIS foren més altes en el grup amb SDRA. En el grup de pacients amb SDRA, 8 (50%) dels pacients van tenir en el moment de la mesura una severa SDRA, definida com a PaO2/FiO2 <100 mmHg i 8 (50%) pacients van precisar ECMO. La causa més freqüent de SDRA fou pneumònia amb xoc sèptic (94%). Les concentracions de pentà, malondialdehid, propionaldehid i acetona foren significativament més altes en l’aire expirat dels pacients amb SDRA; igualment, els valors de proteïna C-reactiva, interleuquina-6 i procalcitonina en sang foren més alts que en el grup control. Tres significants models de regressió lineal foren trobats entre les concentracions de VOCs i entre malondialdehid-pentà i PaO2/FiO2. Conclusions: Les concentracions dels productes de peroxidació lipídica més altes en l’aire alveolar dels pacients amb SDRA podrien reflectir la quantitat de dany originat per l’estrés oxidatiu en la SDRA. Cal destacar l’associació lineal entre malondialdehid-pentà i PaO2/FiO2, que suggereix que augments en la concentració de malondialdehid-pentà podrien ser indicadors de progressió de la malaltia. Així doncs, aquests biomarcadors podrien ser útils per la detecció precoç de la SDRA, la monitorització de la seva progressió i l’optimització del tractament. IMR-MS és una nova tècnica no invasiva on-line que permet la detecció de productes de peroxidació lipídica en l’aire exhalat a la capçalera del malalt i sense risc pel pacient. Els nostres resultats són un pas important en la monitorització contínua de l’estat clínic dinàmic en pacients en estat crític.
Background: In the setting of acute respiratory distress syndrome (ARDS), activated neutrophils migrate from pulmonary capillaries into the alveolar and interstitial spaces, where they release oxygen free radicals called reactive oxygen species (ROS). ROS play a major role in the pathogenesis of ARDS. The secretion of ROS and other proinflammatory mediators leads to damage to alveolar-capillary membrane, causing increased permeability and pulmonary edema. When ROS interact with lipids from pulmonary cell membranes, a process termed lipid peroxidation takes place, ultimately resulting in the generation of volatile organic compounds (VOCs) such as pentane, malondialdehyde, propionaldehyde, and acetone. Since these compounds are volatile and originate primarily in the lung, they would be expected to be found in exhaled breath earlier than in the blood. Objectives: The primary endpoint was to determine whether the above-mentioned lipid peroxidation products can be measured online in expiratory air of patients with ARDS and whether their concentrations are higher than in a control group without acute lung injury. Secondary endpoints were to determine i) the systemic inflammatory response measured by C-reactive protein, interleukin-6, and procalcitonin in blood; ii) whether there is a linear association between the concentrations of different VOCs and between VOCs and systemic inflammatory markers, as well as between VOCs and lung injury severity expressed by the Lung Injury Score (LIS) and PaO2/FiO2 ratio. Design: A cross-sectional analysis of VOCs and systemic inflammatory markers within a prospective observational descriptive study of clinical parameters conducted from 2009 to 2011. Setting: A 20-bed medical-surgical intensive care unit in a university hospital. Patients: We prospectively enrolled patients with ARDS (within the first 48h of diagnosis) (n=16) and mechanically ventilated patients without acute lung injury and without alveolar infiltrates on chest radiograph (n=14) anytime after admission. ARDS patients were ventilated according to ARDS-Network guidelines. We recorded demographic, physiologic, clinical, radiographic, and biochemical parameters. The severity of the disease at the time of exhaled breath measurement was assessed using the Simplified Acute Physiological Score (SAPS II) and LIS. Extracorporeal lung assist therapy (extracorporeal membrane oxygenation (ECMO) or pumpless interventional lung assist (iLA)) was considered for ARDS patients who did not response to optimal standard treatment. Intervention: The very low concentration of VOCs in exhaled breath requires a supersensitive method to detect them. To this end, we used ion-molecule reaction mass spectrometry (IMR-MS). This technique enables noninvasive real-time observation of sampling. Controlled alveolar air samples obtained using CO2 threshold triggering were analyzed by connecting patients to the IMR-MS via a T-piece inserted between the endotracheal tube and the Y-connector of the respirator. Inspiratory air samples were obtained via a T-piece placed directly in the respiratory circuit. Biochemical and biological parameters in blood were analyzed at the time of the mass spectrometry measurement. Main results: No significant differences in age, sex, body mass index, or comorbidities proportion were found between the two groups. As expected, LIS and SAPS II scores were higher in the ARDS group. In the ARDS group, 8 (50%) patients had severe ARDS defined as PaO2/FiO2 ratio < 100 mmHg at the time of measurement, and 8 (50%) patients underwent ECMO. The most frequent cause of the development of ARDS was pneumonia with septic shock (94%). ARDS patients had significantly higher concentrations of pentane, malondialdehyde, propionaldehyde, and acetone in expiratory air, as well as significantly higher values for C-reactive protein, procalcitonin, and interleukin-6 in blood than the control group. Three significant linear regression models were found between the concentrations of VOCs and between malondialdehyde-pentane and PaO2/FiO2 ratio. Conclusions: The higher concentrations of lipid peroxidation products in alveolar gas samples in ARDS patients may reflect the amount of oxidative stress damage in ARDS. Importantly, the linear association between malondialdehyde-pentane and PaO2/FiO2 ratio suggests that an increase in malondialdehyde-pentane concentrations might be able to detect disease progression. These biomarkers might be useful for detecting ARDS early, monitoring disease progression, and optimizing treatment. IMR-MS is a novel online noninvasive approach that enables real-time detection of lipid peroxidation products in exhaled breath at the bedside without risk to the patient. Our results are an important step in the continuous monitoring of the dynamic clinical status in critically ill patients.
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Retamal, Montes Jaime. « Aspects on ventilation induced stress and strain on regional and global inflammation in experimental acute respiratory distress syndrome ». Doctoral thesis, Uppsala universitet, Anestesiologi och intensivvård, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-296952.

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Mechanical ventilation (MV) is a life-saving therapy in acute respiratory distress syndrome (ARDS), a condition that affects 3000 patients/year in Sweden with a mortality rate of about 40%. However, MV may induce or worsen lung injury causing “ventilator-induced lung injury (VILI)”. From a mechanical perspective strain (deformation, or relative change in lung volume) and stress (tension) have been postulated as main determinants of VILI. High respiratory rate is potentially another factor that may exacerbate VILI by amplifying the total energy transmitted to the lungs during MV. In this thesis in animal ARDS models the hypotheses were that 1) lung parenchyma inhomogeneities concentrate stress and amplify lung damage and inflammation, 2) higher respiratory rates increase lung inflammation and lung edema in heterogeneous ARDS, and 3) local lung deformation is related to local inflammation. First, in a rat model the effect on inflammation and structural damage of regional lung collapse on the healthy surrounding lung tissue was assessed. Second, in porcine models the effect of respiratory rate on lung edema and inflammation was studied during two ventilatory modes; a) a permissive collapse mode and b) a homogenized lung parenchyma mode. Finally, lung deformation was correlated with lung inflammation assessed by positron emission tomography using 18F-FDG uptake. It was found that; 1) local inhomogeneities can act as stress amplifiers, increasing lung tissue inflammation and damage in the healthy surrounded lung. 2) high respiratory rate increases lung edema but decreases lung inflammation when permissive lung collapse is used and that these effects are prevented with lung parenchyma homogenization; 3) local lung deformation and inflammation are well correlated. In conclusion, lung inhomogeneities may aggravate VILI, respiratory rate may affect in different ways VILI progression depending on the ventilatory strategy, and finally, lung deformation is closely related to lung inflammation. With the caveat that the studies are performed in animal models, the results suggest that using ventilator strategies that homogenize the lungs, i.e., open collapsed lung regions and prevent re-collapse in ARDS will reduce VILI and in the end may decrease morbidity and the high mortality in this condition.
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Craven, Thomas Henry John. « Resolving uncertainty in acute respiratory illness using optical molecular imaging ». Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/29507.

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Ventilator associated pneumonia (VAP) and acute respiratory distress syndrome (ARDS) are two respiratory conditions unique to mechanically ventilated patients. The diagnosis of these conditions, and therefore any subsequent treatment, are befuddled by uncertainty. VAP rates vary considerably according to the diagnostic or surveillance criteria used. The pathogenesis of ARDS is well understood but when the internationally agreed consensus criteria are employed, the histological hallmarks are absent about half the time, indicating a disconnection between the clinical diagnosis and what is known about the biology of this condition. It is argued that tests of biological function should be considered in addition to clinical characteristics in order to improve the utility of diagnosis. Given that the pathological sequelae of both VAP and ARDS are driven by an over exuberant host neutrophil response, the activated neutrophil was selected as a potential biological imaging target. Optical molecular imaging uses visible and near visible wavelengths from the electromagnetic spectrum to derive or visualize information based on the optical properties of the target tissue. Optical wavelengths are safe and cheap to work with, producing much higher resolution images than those relying on x-rays or gamma radiation. The imaging modality can be coupled with exogenously applied chemistry to identify specific biological targets or processes. The hypothesis that optical molecular imaging could be used to detect activated neutrophils in real time in the alveolar region of patients was tested. A bespoke optical molecular imaging agent called Neutrophil Activation Probe (NAP), designed in-house, was used to test the hypothesis. NAP is a dendrimeric compound delivered to the alveolar region of a patient in microdoses (≤100 micrograms), becoming fluorescent only on contact with activated neutrophils, and can be detected by optical endomicroscopy. Both the imaging agent and the endomicroscope are delivered to the distal lung via routine bronchoscopy. The agent was tested extensively in the laboratory to demonstrate function, specificity, and safety. Ex vivo testing took place using human and ovine lungs. A regulated dose escalation Phase I clinical trial of investigational medicinal product (CTIMP) in healthy volunteers, patients with bronchiectasis, and mechanically ventilated patients with a pulmonary infiltrate on chest radiography (NCT01532024) was designed and conducted. The aim of the Phase I study was to demonstrate the safety of the technique and to confirm proof of concept. In order to support the requirement for a technique that interrogates alveolar neutrophils two supplementary clinical studies were performed. Firstly, two VAP surveillance techniques (CDC surveillance and HELICS European VAP surveillance) were compared with clinically diagnosed VAP across consecutive admissions in two large tertiary centres for one year. Secondly, the utility of circulating neutrophils to permit discrimination between acute respiratory illnesses was examined. Blood samples from mechanically ventilated patients with and without ARDS underwent flow cytometric assessment using eight clusters of differentiation and internal markers of activation to determine neutrophil phenotype. All clinical studies received the appropriate regulatory, ethical, and/or Caldicott guardian approval prior to commencement. NAP became fluorescent only in the presence of three processes specific to neutrophil activation: active pinocytosis, progressive alkalinization of the phagolysosome, and the activity of human neutrophil elastase. High optical signal was detected following the application of NAP in the alveolar regions of explanted lungs from patients with cystic fibrosis, known to be rich in activated neutrophils. Using an ex vivo ovine lung ventilation and perfusion model optical signal was demonstrated following segmental lung injury. The safety and specificity of the technique in a small cohort of healthy volunteers and mechanically ventilated patients was demonstrated. The technique was tested on a small cohort of patients with bronchiectasis, which provided the first opportunity to obtain broncho-alveolar lavage samples for laboratory correlation. Fluorescent signal was shown in the lavaged neutrophils, labeling that could only have taken place in the alveolar region. The supportive clinical studies found the concordance between actual VAP events was virtually zero even though the reported VAP rates were similar. Furthermore, the rate at which clinicians initiate antibiotics for VAP was approximately five times higher than either surveillance VAP rate. The study of circulating neutrophils from the blood of healthy volunteers and mechanically ventilated patients with and without ARDS indicated circulating neutrophil activation phenotype was not capable of discriminating between clinically diagnosed ARDS and other acute respiratory illnesses. In summary, an ambitious programme of work was completed to develop and support an optical molecular imaging technique that meets the rigorous requirements for human application and can be applied at the bedside to yield immediate visual results. The spatiotemporal relationship of neutrophil activation in real time both in the laboratory and in volunteers and patients was visualized. The visualization of neutrophil activation at such a resolution has never been achieved before in humans, healthy or unhealthy. The Phase I study was not powered to determine utility but recruitment has begun to a Phase II CTIMP (NCT02804854) to investigate the utility, accuracy, and precision of the imaging technique in a large cohort of mechanically ventilated patients. Ultimately, it is proposed that the technique will facilitate diagnosis, stratify patients for treatment and monitor treatment response using this technique.
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Tsang, Hing-pang Clement, et 曾慶鵬. « The effectiveness of extracorporeal membrane oxygenation for pandemic influenza A (H1N1) induced acute respiratory distress syndrome in adults ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193823.

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Given that pandemic swine flu outbreak led to substantial admission in intensive care unit, extracorporeal membrane oxygenation has been increasingly applied to those who suffered from H1N1 infection induced acute respiratory distress syndrome. This review is going to evaluate the effectiveness of using ECMO based on five related observational studies. The result, discussion and policy implication in Hong Kong are discussed. Since the ECMO system has been technological improved in recent years, there are less complications when applying ECMO. In view of evidence of reviewed studies, application of ECMO in Hong Kong can be considered as cost effective. And since only a few hospitals in Hong Kong can offer ECMO application, retrieval teams are needed to ensure safety transfer between hospitals.
published_or_final_version
Public Health
Master
Master of Public Health
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Johansson, Joakim. « Function of granulocytes after burns and trauma, associations with pulmonary vascular permeability, acute respiratory distress syndrome, and immunomodulation ». Doctoral thesis, Linköpings universitet, Institutionen för klinisk och experimentell medicin, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-94513.

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Background: Our innate immunesystem protects us from infections but, since its methods is not all specific for microorganisms, may also induce collateral damage. Severe physical injury often proved deadly throughout evolution. Such injuries may induce massive collateral damage. Nowadays we can initiate advanced critical care for affected patients and save them from imminent trauma-related death. We are therefore faced with the fact that the collateral damage from the immune system may pose a major threat to the patient, the pathophysiology of which is not amenable to direct medical treatment and which leaves us with only passive supportive measures. In this thesis we investigated the role of leucocytes under such circumstances. Our main aim was to understand better the role of leucocytes in the development of increased vascular permeability after burns and trauma. More specifically we investigated the impact of an injury on the function of leucocytes such as the dynamic change of certain cell-surface receptors on the leucocytes and in their numbers and immature forms. We wanted to find out if the increased pulmonary vascular permeability after a burn could be mediated through heparin binding protein (HBP) released from granuloctes, and whether HBP could be used as a biomarker for respiratory failure after trauma. We also wanted to confirm the possible role of histamine as a mediator of the systemic increase in vascular permeability after burns. Methods: The dynamic change of cell-surface receptors was measured by flow-acquired cytometer scanning (FACS) on blood samples taken after burns. The concentrations of HBP after a burn and mechanical trauma were analysed in plasma. Pulmonary vascular permeability after a burn was assessed using transpulmonary thermodilution. The histamine turnover after a burn was assessed with high performance liquid chromatography (HPLC) for concentrations of histamine and methylhistamine in urine. Results: We confirmed earlier investigations showing altered expression of receptors on leucocytes after a burn, receptors intimately associated with leucocyte functions (study I). In a pilot study of 10 patients we measured plasma concentrations of HBP and found them to be increased soon after a burn (study II). This finding was not confirmed in a larger, more extensive and specific study of 20 patients. We did, however, find an association between alterations in the number of leucocytes soon after a burn and pulmonary vascular permeability, indicating that they had a role in this process (study III). In another study of trauma (non burn) we found an association between the concentration of HBP in early plasma-samples after injury and the development of ARDS, indicating that granulocytes and HBP have a role in its aetiology (study IV). We found a small increase in urinary histamine and normal urinary methylhistamine concentrations but had anticipated a distinct increase followed by a decrease after reading the current papers on the subject. This indicates that the role of histamine as a mediator of increased vascular permeability after burns may have been exaggerated (study V). Conclusions: We conclude that leucocytes are affected by burns and trauma, and it is likely that they contribute to the development of respiratory failure and acute respiratory distress syndrome (ARDS). HBP is a candidate biomarker for the early detection of ARDS after trauma, and the white blood count (WBC) is a useful biomarker for the detection of decreased oxygenation soon after a burn.
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Robinson, Bryce RH M. D. « Implications of acute resuscitation and mechanical ventilation strategies upon pulmonary complications following injury ». University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1427882608.

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Hirani, Nikhil A. « The regulation of interleukin-8 from macrophages by acute hypoxia and hyperoxia : a role in the pathogenesis of the acute respiratory distress syndrome (ARDS) ». Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/28236.

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Adequate oxygenation is a critical requirement for normal cellular function in humans. In patients with conditions such as major trauma, sepsis and aspiration injury there is often significant local and widespread tissue hypoxia as a consequence of inadequate oxygen supply or impaired oxygen utilisation. In this thesis, the role of acute hypoxia and hyperoxia were investigated in a novel animal model of acute lung injury. Bronchoscopic instillation of HC1 acid in an anaesthetised, ventilated rabbit resulted in reproducible acute neutrophilic lung injury in the instilled lobe. The contra-lateral lung acted as a site of potential indirect lung injury. Systemic hypoxaemia was induced by reduction in the inspiratory oxygen fraction. Compared to normoxic controls (arterial PaO2 ~ 11 KPa), acute hypoxia (PaO2 ~ 5 KPa) for up to 2 hours increased intrapulmonary IL-8 mRNA, but not protein expression in the acid-injured lung. Delivery of 100% oxygen for 2 hours (PaO2 ~ 60 KPa) following acute hypoxia, increased both intrapulmonary IL-8 mRNA and IL-8 protein levels. The increase in IL-8 protein was attenuated if the reoxygenation phase was controlled to return arterial PO2 to normoxic levels (~ 11 KPa). Acute hypoxia/hyperoxia may represent a potential mechanism by which intrapulmonary IL-8 levels are rapidly raised in patients at-risk of ARDS. In human blood monocyte derived macrophages, it was shown that acute hypoxia alone rapidly upregulated IL-8 gene expression. A number of other proinflammatory cytokines were conversely down regulated by hypoxia. The IL-8 increase occurred in association with raised nuclear levels of AP-1 and C/EBP-β, but not NF-κB. Hypoxia induced expression of the transcription factor HIF-1α. However cobalt chloride and desferroxamine, HIF-1α-inducing hypoxia mimics, did not upregulate IL-8, suggesting that IL-8 regulation was HIF-1 independent. Both the pattern of chemokine expression and transcription factor activation with hypoxia differed from that induced by lipopolysaccharide (LPS), an archetypal pathogenic stimulus.
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30

Chuang, Jiin-Haur. « Acute respiratory distress syndrome in septic shock : the role of endogenous opiates and the effect of an opioid antagonist ». Thesis, McGill University, 1985. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=65382.

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31

Plouffe, Jannell. « Development of an evidence-based clinical practice guideline for prone positioning in acute respiratory distress syndrome for the pediatric patient ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ62825.pdf.

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Bassford, Christopher R. « 11β-hydroxysteroid dehydrogenase glucocorticoid metabolism within the lung and its influence on macrophage function in the acute respiratory distress syndrome ». Thesis, University of Warwick, 2011. http://wrap.warwick.ac.uk/49584/.

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The acute respiratory distress syndrome (ARDS) is an important cause of respiratory failure in critically ill patients characterised by severe inflammation within the lungs. This inflammation is limited by anti-­inflammatory glucocorticoid hormones released from the hypothalamus-pituitary-adrenal (HPA) system. This thesis reports a series of investigations into glucocorticoid concentrations and glucocorticoid metabolism within the lungs of patients with ARDS. It also contains an investigation into a potential biomarker for ARDS. Our study of glucocorticoid concentrations in alveolar epithelial lining fluid showed increased cortisol concentrations within the lungs at onset of ARDS. These concentrations have a positive relationship with critical illness severity indices, but negative relationships with alveolar permeability and alveolar neutrophil counts. In peripheral tissues cortisone and cortisol are inter-converted by iso-­enzymes of 11β-­hydroxysteroid dehydrogenase (11β-­HSD). We have shown that healthy primary resident alveolar macrophages increase their production of active cortisol by the oxo-­reduction of inactive cortisone in response to inflammatory stimuli. Alveolar macrophages are responsible for the removal of spent and apoptotic inflammatory cells, failure of this process causes further inflammation. We have shown that glucocorticoids increase the rate of uptake of apoptotic cells by alveolar macrophages, and that macrophage 11β-HSD production of cortisol increases this process. We have shown however that alveolar macrophages extracted from patients with established ARDS have decreased 11β-HSD oxo-reductase activity. This decreased conversion of cortisone to cortisol will cause a diminished response to the anti-inflammatory signal of the HPA system. The implications of this are that they will have a limited capacity to up-­regulate efferocytosis and a diminished anti-­inflammatory potential. The receptor for advanced glycation end-­products (RAGE) is a potential biomarker in ARDS. We have shown that RAGE concentrations in plasma and BALF had excellent diagnostic compatibility with ARDS diagnostic criteria. The use of a threshold RAGE concentration could assure pulmonary inflammation in future investigations.
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33

Witte, Esther [Verfasser], et Jörg [Akademischer Betreuer] Reutershan. « Die Bedeutung des Adenosinrezeptors A2B bei der Migration neutrophiler Granulozyten im Acute Respiratory Distress Syndrome / Esther Witte ; Betreuer : Jörg Reutershan ». Tübingen : Universitätsbibliothek Tübingen, 2013. http://d-nb.info/1160683530/34.

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34

Campos, Fábio Joly [UNESP]. « Efeito do óxido nítrico inalatório associado à ventilação mecânica protetora na lesão pulmonar aguda induzida experimentalmente ». Universidade Estadual Paulista (UNESP), 2011. http://hdl.handle.net/11449/92154.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Fundamentação/Objetivos: Síndrome do desconforto respiratório agudo (SDRA) cursa com elevada taxa de mortalidade a despeito do melhor entendimento de sua fisiopatologia e recentes avanços no tratamento. Ventilação mecânica (VM), uma das mais importantes formas de tratamento, é baseada na utilização de estratégias protetoras com baixo volume corrente (VC) e elevada pressão expiratória final positiva (PEEP). Existem várias terapias adjuvantes, entre as quais o óxido nítrico inalatório (NOi) é conhecido por suas propriedades antiinflamatórias e efeitos benéficos sobre a oxigenação. Quando o NOi é associado à VM protetora, o gás poderia não apenas melhorar a oxigenação mas também reduzir a lesão pulmonar. Objetivo: comparar a VM protetora, com e sem NOi, quanto a oxigenação, estresse oxidativo do tecido pulmonar e lesão histológica e inflamatória dos pulmões. Métodos: Trinta coelhos foram instrumentados com traqueotomia e acessos vasculares e ventilados com FiO2 de 1,0. Lesão pulmonar aguda (LPA) foi induzida por infusão traqueal de salina aquecida (30mL/Kg, 38°C) e o estresse oxidativo do tecido pulmonar foi medido pelo método da capacidade antioxidante total (TAP). A inflamação pulmonar foi avaliada pelo contagem do número de células polimorfonucleares (PMN) recuperadas do fluido de lavagem broncoalveolar (BAL). Também foi analisado um escore de lesão pulmonar histopatológica. Os animais foram distribuídos nos seguintes grupos, cada um dos quais com 10 coelhos: a) Controle (GC): baixo VC (6mL/Kg) e PEEP de 5cmH2O; b) ventilação mecânica protetora + LPA (GVM): baixo VC (6mL/Kg) e PEEP de 10cmH2O; e c) ventilação mecânica protetora + LPA + NOi (GVM-NO): baixo VC (6mL/Kg), PEEP de 10cmH2O, e NOi de 5ppm.; d) Dez animais não instrumentados e não ventilados mecanicamente, grupo sadio (GSadio), foram estudados para o TAP. Pressão...
Background/Objectives: Acute respiratory distress syndrome (ARDS) has been associated with high mortality rate despite better understanding of its pathophysiology and recent advances in treatment. Mechanical ventilation (MV), one of the most important treatments, is based on using protective strategies with low tidal volume (VT) and high positive end expiratory pressure (PEEP). There are also many adjunctive therapies, of which inhaled nitric oxide (iNO) is known for its antiinflammatory properties and positive effects on oxygenation. When iNO is associated with protective MV, it could not only improve oxygenation but may also reduce lung injury. Objective: to compare protective MV with and without iNO for oxygenation, lung oxidative stress, inflammatory and histopathological injury. Methods: Thirty rabbits were instrumented with a tracheotomy and vascular catheters and ventilated at FiO2 1.0. Acute lung injury (ALI) was induced by tracheal infusion of warm saline (30mL/Kg, 38°C), lung oxidative stress was assessed by total antioxidant performance (TAP) assay, and pulmonary inflammation was assessed by counting of the number of polymorphonuclear leukocyte (PMN) in bronchoalveolar lavage fluid (BAL). Histopathological lung injury was assessed by a lung injury score. Animals were assigned to groups: a) Control (CG): low tidal volume (6mL/Kg) and PEEP 5cmH2O; b) ALI without iNO (LIG): low tidal volume (6mL/Kg) and PEEP 10cmH2O; and c) ALI with iNO (LINOG): low tidal volume (6mL/Kg), PEEP 10cmH2O, and iNO 5ppm; d) Ten rabbits were studied for oxidative stress analysis without ALI and MV, healthy group (HG). Ventilatory and hemodynamic parameters were recorded every 30 minutes for 4 hours. Statistical significance was set at p<0.05. Results: After induction, ALI groups were similar but worse than CG for PaO2/FiO2 (CG:438±87>LIG:80±13=LINOG:81±24;p<0.05) and pulmonary compliance... (Complete abstract click electronic access below)
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35

Gusman, Pablo Braga [UNESP]. « Distribuição regional de gás e tecido na síndrome da angústia respiratória aguda : consequências do efeito da pressão expiratória final positiva ». Universidade Estadual Paulista (UNESP), 2007. http://hdl.handle.net/11449/100145.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Desde sua primeira descrição, muito se investiu no melhor conhecimento da SARA, na identificação de sua etiologia, seus fatores de risco, seus mecanismos e mediadores, escolhendo-se métodos críticos de avaliação clínica que também pudessem definir o prognóstico. Com o objetivo de verificar se os efeitos da PEEP dependem da morfologia pulmonar, comparando sua resposta em três grupos de pacientes, descritos de acordo com os aspectos de hiperdensidades observadas nos cortes tomográficos, foram estudados 71 pacientes portadores de SARA, comparando-os a 11 voluntários sadios. Cada paciente foi submetido a exame tomográfico helicoidal de tórax em ZEEP e após implemento de PEEP de 10 cmH2O. Parâmetros hemodinâmicos e respiratórios foram mensurados nas mesmas condições. Hiperdistensão induzida pela PEEP e recrutamento alveolar foram quantificados por um software específico, Lungview®. Hiperdistensão ocorreu somente nos lobos superiores e se correlacionou significativamente com volume pulmonar caracterizado por uma densidade tomográfica de parênquima pulmonar variando entre -900 UH e -800 UH em ZEEP. Efeitos cárdio-respiratórios em PEEP foram semelhantes nos pacientes com SARA primária e secundária. O recrutamento alveolar induzido pela PEEP nos lobos inferiores se correlacionou de forma significativa com seu volume pulmonar residual. Recrutamento alveolar induzido pela PEEP foi maior nos lobos inferiores com atelectasias inflamatórias do que nos lobos inferiores com atelectasias mecânicas. A morfologia pulmonar acessada pelo exame tomográfico influenciou de forma significativa os efeitos da PEEP. Em pacientes com hiperdensidades difusas, a PEEP induziu recrutamento alveolar importante sem hiperdistensão, enquanto que nos pacientes com hiperdensidades localizadas, a PEEP induziu...
There has been some decades, a lot has been invested in the attempt of better knowledge of ARDS, characterizing in a more trustworthy way your aetiology, risk factors, its mechanisms and mediators, choosing critical methods of clinical evaluation that could also foresee the prognostic. To determine whether differences in lung morphology assessed on the CT scan influence the response to PEEP we study by a prospective study during a 53-month period in a fourteenbed surgical Intensive Care Unit of a university hospital, seventy-one consecutive patients with early ARDS. In each patient, a fast spiral thoracic CT scan was performed in ZEEP and after implementation of PEEP 10 cmH2O. Hemodynamic and respiratory parameters were also measured in the same conditions. PEEPinduced overdistension and alveolar recruitment were quantified by a specifically designed software, Lungview®. Overdistension occurred only in the upper lobes and was significantly correlated with the volume of lung characterized by a scanographic density ranging between -900 HU and -800 HU parenchyma in ZEEP conditions. Cardiorespiratory effects of PEEP were similar in patients with primary and secondary ARDS. PEEP-induced alveolar recruitment of lower lobes was significantly correlated with their resting lung volume. PEEP-induced alveolar recruitment was greater in the lower lobes with inflammatory atelectasis than in the lower lobes with mechanical atelectasis. Lung morphology assessed on the CT scan markedly influenced the effects of PEEP: in patients with diffuse hyperdensities, PEEP induced a marked alveolar recruitment without overdistension whereas, in patients with lobar hyperdensities, PEEP induced a mild alveolar recruitment associated with overdistension of previously aerated lung areas. These results... (Complete abstract click eletronic address below)
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Selke, Maren Verena [Verfasser], Michael [Akademischer Betreuer] Quintel, Sven [Akademischer Betreuer] Kantelhardt et Patricia [Akademischer Betreuer] Virsik-köpp. « Interaktionen zwischen "Acute Intracranial Hypertension" und "Acute Respiratory Distress" Syndrome : Auswirkungen auf den hypoxiesensiblen Hippocampus / Maren Verena Selke. Gutachter : Michael Quintel ; Sven Kantelhardt ; Patricia Virsik-Köpp. Betreuer : Michael Quintel ». Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2011. http://d-nb.info/1042733988/34.

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Campos, Fabio Joly. « Efeito do óxido nítrico inalatório associado à ventilação mecânica protetora na lesão pulmonar aguda induzida experimentalmente / ». Botucatu : [s.n.], 2011. http://hdl.handle.net/11449/92154.

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Orientador: José Roberto Fioretto
Banca: Ana Lúcia dos Anjos Ferreira
Banca: Regina Grigolli Cesar
Resumo: Fundamentação/Objetivos: Síndrome do desconforto respiratório agudo (SDRA) cursa com elevada taxa de mortalidade a despeito do melhor entendimento de sua fisiopatologia e recentes avanços no tratamento. Ventilação mecânica (VM), uma das mais importantes formas de tratamento, é baseada na utilização de estratégias protetoras com baixo volume corrente (VC) e elevada pressão expiratória final positiva (PEEP). Existem várias terapias adjuvantes, entre as quais o óxido nítrico inalatório (NOi) é conhecido por suas propriedades antiinflamatórias e efeitos benéficos sobre a oxigenação. Quando o NOi é associado à VM protetora, o gás poderia não apenas melhorar a oxigenação mas também reduzir a lesão pulmonar. Objetivo: comparar a VM protetora, com e sem NOi, quanto a oxigenação, estresse oxidativo do tecido pulmonar e lesão histológica e inflamatória dos pulmões. Métodos: Trinta coelhos foram instrumentados com traqueotomia e acessos vasculares e ventilados com FiO2 de 1,0. Lesão pulmonar aguda (LPA) foi induzida por infusão traqueal de salina aquecida (30mL/Kg, 38°C) e o estresse oxidativo do tecido pulmonar foi medido pelo método da capacidade antioxidante total (TAP). A inflamação pulmonar foi avaliada pelo contagem do número de células polimorfonucleares (PMN) recuperadas do fluido de lavagem broncoalveolar (BAL). Também foi analisado um escore de lesão pulmonar histopatológica. Os animais foram distribuídos nos seguintes grupos, cada um dos quais com 10 coelhos: a) Controle (GC): baixo VC (6mL/Kg) e PEEP de 5cmH2O; b) ventilação mecânica protetora + LPA (GVM): baixo VC (6mL/Kg) e PEEP de 10cmH2O; e c) ventilação mecânica protetora + LPA + NOi (GVM-NO): baixo VC (6mL/Kg), PEEP de 10cmH2O, e NOi de 5ppm.; d) Dez animais não instrumentados e não ventilados mecanicamente, grupo sadio (GSadio), foram estudados para o TAP. Pressão... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Background/Objectives: Acute respiratory distress syndrome (ARDS) has been associated with high mortality rate despite better understanding of its pathophysiology and recent advances in treatment. Mechanical ventilation (MV), one of the most important treatments, is based on using protective strategies with low tidal volume (VT) and high positive end expiratory pressure (PEEP). There are also many adjunctive therapies, of which inhaled nitric oxide (iNO) is known for its antiinflammatory properties and positive effects on oxygenation. When iNO is associated with protective MV, it could not only improve oxygenation but may also reduce lung injury. Objective: to compare protective MV with and without iNO for oxygenation, lung oxidative stress, inflammatory and histopathological injury. Methods: Thirty rabbits were instrumented with a tracheotomy and vascular catheters and ventilated at FiO2 1.0. Acute lung injury (ALI) was induced by tracheal infusion of warm saline (30mL/Kg, 38°C), lung oxidative stress was assessed by total antioxidant performance (TAP) assay, and pulmonary inflammation was assessed by counting of the number of polymorphonuclear leukocyte (PMN) in bronchoalveolar lavage fluid (BAL). Histopathological lung injury was assessed by a lung injury score. Animals were assigned to groups: a) Control (CG): low tidal volume (6mL/Kg) and PEEP 5cmH2O; b) ALI without iNO (LIG): low tidal volume (6mL/Kg) and PEEP 10cmH2O; and c) ALI with iNO (LINOG): low tidal volume (6mL/Kg), PEEP 10cmH2O, and iNO 5ppm; d) Ten rabbits were studied for oxidative stress analysis without ALI and MV, healthy group (HG). Ventilatory and hemodynamic parameters were recorded every 30 minutes for 4 hours. Statistical significance was set at p<0.05. Results: After induction, ALI groups were similar but worse than CG for PaO2/FiO2 (CG:438±87>LIG:80±13=LINOG:81±24;p<0.05) and pulmonary compliance... (Complete abstract click electronic access below)
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Mendler, Marc Robin [Verfasser]. « Einfluss von permissiver Hyperkapnie auf den Gasaustausch, die Lungenschädigung und die Hämodynamik am Versuchstier mit schwerem "Acute Respiratory Distress Syndrome (ARDS)" / Marc Robin Mendler ». Ulm : Universität Ulm. Medizinische Fakultät, 2014. http://d-nb.info/1046890174/34.

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Doolittle, Lauren May. « The Impact of Alveolar Type II Cell Mitochondrial Damage and Altered Energy Production on Acute Respiratory Distress Syndrome Development During Influenza A Virus Infection ». The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu159224389333959.

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Kanzler, Stephanie Sarah Verfasser], Stefan [Akademischer Betreuer] Uhlig et Gabriele [Akademischer Betreuer] [Pradel. « A murine two-hit model to investigate the early time-course of inflammation in acute respiratory distress syndrome / Stephanie Sarah Kanzler ; Stefan Uhlig, Gabriele Pradel ». Aachen : Universitätsbibliothek der RWTH Aachen, 2021. http://d-nb.info/1238081312/34.

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Gusman, Pablo Braga. « Distribuição regional de gás e tecido na síndrome da angústia respiratória aguda : consequências do efeito da pressão expiratória final positiva / ». Botucatu : [s.n.], 2007. http://hdl.handle.net/11449/100145.

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Orientador: Luiz Antonio Vane
Banca: Yara Marcondes Machado Castiglia
Banca: José Reinaldo Cerqueira Braz
Banca: José Luiz Gomes do Amaral
Banca: Sílvia Regina Rios Vieira
Resumo: Desde sua primeira descrição, muito se investiu no melhor conhecimento da SARA, na identificação de sua etiologia, seus fatores de risco, seus mecanismos e mediadores, escolhendo-se métodos críticos de avaliação clínica que também pudessem definir o prognóstico. Com o objetivo de verificar se os efeitos da PEEP dependem da morfologia pulmonar, comparando sua resposta em três grupos de pacientes, descritos de acordo com os aspectos de hiperdensidades observadas nos cortes tomográficos, foram estudados 71 pacientes portadores de SARA, comparando-os a 11 voluntários sadios. Cada paciente foi submetido a exame tomográfico helicoidal de tórax em ZEEP e após implemento de PEEP de 10 cmH2O. Parâmetros hemodinâmicos e respiratórios foram mensurados nas mesmas condições. Hiperdistensão induzida pela PEEP e recrutamento alveolar foram quantificados por um software específico, Lungview®. Hiperdistensão ocorreu somente nos lobos superiores e se correlacionou significativamente com volume pulmonar caracterizado por uma densidade tomográfica de parênquima pulmonar variando entre -900 UH e -800 UH em ZEEP. Efeitos cárdio-respiratórios em PEEP foram semelhantes nos pacientes com SARA primária e secundária. O recrutamento alveolar induzido pela PEEP nos lobos inferiores se correlacionou de forma significativa com seu volume pulmonar residual. Recrutamento alveolar induzido pela PEEP foi maior nos lobos inferiores com atelectasias inflamatórias do que nos lobos inferiores com atelectasias mecânicas. A morfologia pulmonar acessada pelo exame tomográfico influenciou de forma significativa os efeitos da PEEP. Em pacientes com hiperdensidades difusas, a PEEP induziu recrutamento alveolar importante sem hiperdistensão, enquanto que nos pacientes com hiperdensidades localizadas, a PEEP induziu... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: There has been some decades, a lot has been invested in the attempt of better knowledge of ARDS, characterizing in a more trustworthy way your aetiology, risk factors, its mechanisms and mediators, choosing critical methods of clinical evaluation that could also foresee the prognostic. To determine whether differences in lung morphology assessed on the CT scan influence the response to PEEP we study by a prospective study during a 53-month period in a fourteenbed surgical Intensive Care Unit of a university hospital, seventy-one consecutive patients with early ARDS. In each patient, a fast spiral thoracic CT scan was performed in ZEEP and after implementation of PEEP 10 cmH2O. Hemodynamic and respiratory parameters were also measured in the same conditions. PEEPinduced overdistension and alveolar recruitment were quantified by a specifically designed software, Lungview®. Overdistension occurred only in the upper lobes and was significantly correlated with the volume of lung characterized by a scanographic density ranging between -900 HU and -800 HU parenchyma in ZEEP conditions. Cardiorespiratory effects of PEEP were similar in patients with primary and secondary ARDS. PEEP-induced alveolar recruitment of lower lobes was significantly correlated with their resting lung volume. PEEP-induced alveolar recruitment was greater in the lower lobes with inflammatory atelectasis than in the lower lobes with mechanical atelectasis. Lung morphology assessed on the CT scan markedly influenced the effects of PEEP: in patients with diffuse hyperdensities, PEEP induced a marked alveolar recruitment without overdistension whereas, in patients with lobar hyperdensities, PEEP induced a mild alveolar recruitment associated with overdistension of previously aerated lung areas. These results... (Complete abstract click eletronic address below)
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Boissier, Florence. « Dysfonction vasculaire pulmonaire et ventriculaire droite au cours du SDRA : approche échocardiographique ». Thesis, Paris Est, 2014. http://www.theses.fr/2014PEST0057.

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Contexte: Le syndrome de détresse respiratoire aigüe (SDRA) est associé à une dysfonction vasculaire pulmonaire. Objectifs: Préciser le retentissement cardiaque de cette dysfonction vasculaire pulmonaire en recherchant la fréquence et le pronostic du foramen ovale perméable, du passage transpulmonaire de bulles en échographie de contraste, du cœur pulmonaire aigu (CPA), de la dysfonction systolique ventriculaire droite ainsi que de la déformation ventriculaire gauche au cours du SDRA. Nous avons aussi évalué la tolérance hémodynamique de la ventilation en Pression Expiratoire Positive (PEP) élevée. Méthodes: Les explorations étaient menées par échographie trans-œsophagienne (ETO) traditionnelle et en signature acoustique. Résultats: La faisabilité de l'ETO en décubitus ventral est bonne. Le foramen ovale perméable, détecté chez 19% des patients, est associé à une moins bonne réponse à l'augmentation de la PEP et à un recours aux thérapeutiques de sauvetage plus fréquent. Le passage de bulles transpulmonaire ne rend pas compte du seul shunt intra-pulmonaire anatomique, et dépend plus des conditions hémodynamiques (augmentation du débit cardiaque associée au sepsis) que de la ventilation. Le CPA, retrouvé chez 22% des patients, est associé à une pression motrice plus élevée, et au sepsis ; il est fréquemment associé à une insuffisance circulatoire, avec une mortalité plus élevée à J28. La quantification de la déformation ventriculaire gauche systolique par l'index d'excentricité est un bon marqueur de CPA, mais pas la dysfonction contractile ventriculaire droite évaluée en signature acoustique. Enfin, nous n'avons pas retrouvé de lien robuste entre la tolérance hémodynamique et l'efficacité respiratoire (recrutement alvéolaire) des niveaux de PEP élevés, sous réserve d'un nombre limité de patients. Conclusion: Les conséquences cardiaques de la dysfonction vasculaire pulmonaire restent fréquentes et associées à un pronostic péjoratif, avec des implications respiratoires et circulatoires
Context: Acute respiratory distress syndrome (ARDS) leads to pulmonary vascular dysfunction Aims: We assessed cardiac consequences of pulmonary vascular dysfunction by detecting patent foramen ovale and transpulmonary bubbles transit using contrast echocardiography, acute cor pulmonale, right ventricle systolic dysfunction and left ventricle deformation during ARDS. We also assessed hemodynamic tolerance of high positive end expiratory pressure (PEEP). Methods: Transesophageal echocardiography (TEE) was performed with standard measurements and speckle tracking. Results: TEE could be safely performed in prone position. Patent foramen ovale was detected in 19% of patients, and was associated with a poor oxygenation response to PEEP, and greater use of adjunctive interventions. Transpulmonary bubbles transit was not solely related to anatomical intrapulmonary shunt, but was merely influenced by hemodynamic status (increased cardiac output associated with sepsis). Acute cor pulmonale occurred in 22% of patients, and was associated with a higher driving pressure and with sepsis; it was often associated with circulatory failure, with higher day-28 mortality. Left ventricle systolic deformation (evaluated by eccentricity index) but not right ventricle contractile impairment (evaluated with speckle tracking) was associated with acute cor pulmonale. Finally, we did not find a robust relation between hemodynamic tolerance and alveolar recruitment with higher PEEP levels, but the limited number of patients restricted the power of the analysis. Conclusion: Cardiac consequences of pulmonary vascular dysfunction remain frequent and associated with a poorer prognosis, with respiratory and circulatory implications
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Rossi, Patrik. « The role of the endothelin system in experimental acute lung injury with special reference to the formation of extra-vascular lung water / ». Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-700-6/.

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Huhle, Robert [Verfasser], de Abreu Marcelo [Gutachter] Gama et Ute [Gutachter] Morgenstern. « Periodic Variable Mechanical Ventilation and Dynamics of Recruitment and De-recruitment in Experimental Acute Respiratory Distress Syndrome / Robert Huhle ; Gutachter : Marcelo Gama de Abreu, Ute Morgenstern ». Dresden : Technische Universität Dresden, 2019. http://d-nb.info/1227833407/34.

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Huhle, Robert [Verfasser], Marcelo Gama de [Gutachter] Abreu et Ute [Gutachter] Morgenstern. « Periodic Variable Mechanical Ventilation and Dynamics of Recruitment and De-recruitment in Experimental Acute Respiratory Distress Syndrome / Robert Huhle ; Gutachter : Marcelo Gama de Abreu, Ute Morgenstern ». Dresden : Technische Universität Dresden, 2019. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa2-364976.

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46

Pereira, Marcelo Luís Monteiro. « O papel da heme oxigenase 1 na síndrome do desconforto respiratório agudo associada à malária ». Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-11112016-154538/.

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A malária é uma doença causada pelo parasita do gênero Plasmodium e que foi responsável por cerca de 440.000 mortes em 2015. A síndrome do desconforto respiratório agudo (SDRA) é uma das principais complicações clínicas da malária. O modelo murino DBA/2 reproduz os sinais clínicos da SDRA observados em humanos, quando infectado com o Plasmodium berghei ANKA. Além disso, altos níveis da enzima heme oxigenase 1 (HO-1) foram observados em casos de malária cerebral e em SDRA em humanos. Os nossos dados indicam que os níveis da HO-1 estão aumentados em camundongos que desenvolvem SDRA associada à malária (SDRA-AM). Adicionalmente, a droga indutora de HO-1 (hemina) aumentou a sobrevivência e preveniu a SDRA-AM. Verificou-se também uma redução na permeabilidade pulmonar e nos níveis de VEGF, além de uma melhoria nos parâmetros respiratórios em animais tratados com hemina. Assim sendo, a indução da HO-1 antes do desenvolvimento da SDRA-AM é protetora e assim, a HO-1 pode ser um alvo de novos fármacos, como forma de prevenir o desenvolvimento da SDRA-AM em humanos.
Malaria is a serious disease, caused by the parasite of the genus Plasmodium, which was responsible to 440,000 deaths in 2015. Acute lung injury/ acute respiratory distress syndrome (ALI/ARDS) is one of the main clinical complications in severe malaria. The murine model DBA/2 reproduces the clinical signs of ALI/ARDS observed in humans, when infected with Plasmodium berghei ANKA. Additionally, high levels heme oxygenase 1 (HO-1) were reported in cases of cerebral malaria and in ALI/ARDS in humans. Our data have indicated that the HO-1 levels are increased in mice that develop malaria associated ALI/ARDS (MA-ALI/ARDS). Additionally, a HO-1 inducing drug (hemin) increased the survival rate and prevented mice from developing MA-ALI/ARDS in treated mice. Also, there was a decrease in the lung permeability and in lung VEGF levels, and an amelioration of respiratory parameters. Therefore, the induction of HO-1 before the development of MA-ALI/ARDS is protective, making this enzyme a possible target of new drugs to prevent the development of MA-ALI/ARDS in humans.
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Carpi, Mario Ferreira [UNESP]. « Efeito imediato e prolongado da administração precoce de óxido nítrico inalatório em crianças portadoras de síndrome do desconforto respiratório agudo ». Universidade Estadual Paulista (UNESP), 2003. http://hdl.handle.net/11449/104678.

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Made available in DSpace on 2014-06-11T19:33:27Z (GMT). No. of bitstreams: 0 Previous issue date: 2003Bitstream added on 2014-06-13T19:44:14Z : No. of bitstreams: 1 carpi_mf_dr_botfm.pdf: 214359 bytes, checksum: 0134d7f3e72fe3bbaff53ae651e657bf (MD5)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
A Síndrome do Desconforto Respiratório Agudo (SDRA) é a forma clínica mais grave da lesão pulmonar aguda e, apesar do melhor entendimento de sua fisiopatologia, a taxa de mortalidade permanece elevada. O óxido nítrico inalatório (NOi) é um vasodilatador seletivo de áreas pulmonares ventiladas, promovendo a otimização da relação ventilação/perfusão nestas áreas, com melhora da oxigenação e facilitação do esvaziamento do ventrículo direito. Tais efeitos permitiriam a redução de parâmetros ventilatórios, habitualmente elevados na SDRA, diminuindo o risco de lesão pulmonar induzida pela ventilação mecânica e a morbi/mortalidade. O estudo teve como objetivos avaliar o efeito imediato e prolongado da administração precoce de NOi associada à terapia convencional sobre a oxigenação e parâmetros ventilatórios, mortalidade, tempo de internação na UTI Pediátrica e duração da ventilação mecânica em crianças portadoras de SDRA. Dois grupos de pacientes pediátricos com SDRA foram comparados: grupo NOi (GNO; n=18), seguido prospectivamente, composto de pacientes que receberam NOi associado à terapia convencional e grupo terapia convencional (GTC; n=21), avaliado retrospectivamente, formado de pacientes que utilizaram apenas terapia convencional. Os critérios para iniciar a administração do NOi foram: saturação arterial de oxigênio < 90% a despeito de uma fração inspirada de oxigênio (FiO2) 0,6 e de uma pressão expiratória final positiva (Peep) 10 cmH2O. A resposta imediata ao NOi foi avaliada em um teste de resposta de quatro horas, considerando resposta positiva um aumento na relação PaO2/FiO2 de 10 mmHg acima dos valores basais. A terapia convencional não foi modificada durante o teste. Nos dias subseqüentes os pacientes que exibiram resposta positiva continuaram recebendo a menor dose de NOi...
Acute respiratory distress syndrome (ARDS) is the most severe manifestation and the end spectrum of acute lung injury. It has been associated with high mortality rate, despite better understanding of its pathophysiology and recent therapeutic advances. Inhalde nitric oxide (iNO)-induced vasodilation of pulmonary vasculature adjacent to well-ventilated alveoli increases blood flow to these lung areas and preferentially shunt blood away from poorly ventilated regions, matching V/Q and reducing intrapulmonary shunt. This results in improved oxygenation and reduction of both pulmonary vascular resistence and right ventricle afterload. By improving V/Q matching, iNO may allow less aggressive mechanical ventilation (MV), which minimizes the risk of ventilator-induced lung injury and mortality. The aims of this study were: 1) to determine the acute and sustained effects of iNO on some oxygenation indexes and ventilator settings, to analyze the weaning process, and to assess the safety of NO inhalation; 2) to test the hypothesis that early administration of iNO would reduce mortality rate, intensive care length of stay, and the duration of MV comparing a group of pediatric ARDS patients treated with iNO plus conventional therapy with another treated only with conventional therapy. Children with ARDS, aged between one month and 12 years were studied. There were two groups: iNO group (iNOG; n=18) composed of patients prospectively enrolled from November 1998 to 2002, and conventional therapy group (CTG; n=21) consisting of historical control patients admitted from August 1996 to August 1998. Study groups were of similar ages, gender, primary diagnoses, pediatric risk of mortality score, and mean airway pressure. PaO2/FiO2 ratio was lower (CTG: 116.9l34.5; iNOG: 71.3l24.1 - p < 0.001) and oxygenation index higher (CTG: 15.2 (7.2-32.2); iNOG: 24.3 (16.3-70.4) - p < 0.001) in the iNOG. Therapy with iNO was introduced as early as 1.5 hours after ARDS.
FAPESP: 01/04971-3
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Scaccabarozzi, D. « THE PATHOGENESIS OF MALARIA ACUTE RESPIRATORY DISTRESS SYNDROME (MA-ARDS) : MODIFICATION OF THE LIPID PROFILE, ANTIOXIDANT DEFENCES AND CYTOKINE CONTENT IN DIFFERENT TISSUES OF MALARIA INFECTED MICE ». Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/231156.

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INTRODUCTION Malaria is a major health problem, with more than 650.000 deaths and 200 million clinical cases each year. Respiratory distress as malaria associated acute respiratory distress syndrome (MA-ARDS) is a common complication. The pathogenesis of MA-ARDS is mainly inflammatory and one of the main observation is the presence of abundant monocytes and macrophages inside the blood capillaries, in the interstitium and also in alveolar spaces. Malaria pigment or haemozoin (Hz) is often seen in these cells reflecting active phagocytosis and leads to the production of cytokines and other inflammatory mediators. Multiple organ dysfunctions are described in MA-ARDS, including liver damages. ARDS in non malarious patients is often associated with disorders of the lung surfactant, which can lead to the increase in surface tension, alveolar collapse and loss of the liquid balance in the lungs. Surfactant is known to reduce the surface tension at the air–liquid interface of lung epithelia and to regulate the local host immune response. It can be separated into a surface active Large Aggregate fractions (LA), representing a reservoir for the surface film located at the air-liquid interface of the alveoli and a less surface active, Small Aggregate fraction (SA). It is not known at present if alterations of the surfactant also exist in MA-ARDS and how they may contribute to the pathology and the development of the inflammatory response. AIM The aim of our studies was to perform a comprehensive analysis of the local and systemic inflammatory response present in MA-ARDS and to analyse the lipid profile of the pulmonary surfactant, the lung and liver tissues and plasma using two different models of murine malaria of similar gravity, but different involvement of lungs or liver. In particular, we studied C57BL/6J mice infected with two different species of Plasmodium: Plasmodium berghei NK65 strain which induces MA-ARDS and Plasmodium chabaudi (PcAS), which does not. The two models allowed us to directly compare the different pathological manifestation of the same infection in order to identify peculiarities which could be exploited for novel therapeutic interventions. RESULTS AND DISCUSSION Macroscopic and functional analysis of lung tissues in the two strains. The lungs of PbNK65 infected mice were swollen, increased in weight and with a dark brown aspect due to micro haemorrhages and to the deposition of Hz clusters in concentrations significantly higher compared to the lungs of mice infected with PcAS. The expression of TNF-α and IFN- was increased only in PbNK65 mice, indicating that these cytokines are induced specifically during MA-ARDS and are not a consequence of malaria infection. This hypothesis was confirmed by the decrease of lung weight and of the CD8+ cells infiltrate, and the reduction /delay in mortality rates seen in PbNK65 mice treated with DEX without a concomitant reduction in parasitaemia. Therefore, DEX seems to ameliorate MA-ARDS, not by inhibiting parasite growth but rather by modulating the immunopathology and the inflammatory response. A significant increase of the total phospholipid (PL) content and cholesterol esters (ChoE) was observed in PbNK65 lungs and was reverted by DEX. Moreover, compared to the control mice (CTR), the fatty acid distribution of lung ChoE was characterized by higher levels of the polyunsaturated fatty acid and an high linoleic/oleic ratio typical of plasma ChoE. All these features confirm a strict correlation between the interstitial oedema and the infiltration of plasma lipoproteins during MA-ARDS. Protein and lipid composition of surfactant and plasma of infected mice. The total bronchoalveolar lavage (BAL) of PbNK65 mice showed a significant increase in the protein levels compared to CTR or PcAS mice, probably due to plasma derived proteins being incorporated into or associated with microstructures in the alveolar hypophase. This event is known to decrease the intrinsic surface activity of surfactant. The total content of PL was not different from CTR, whereas the PL profile of the LA and SA fractions in PbNK65 infected mice showed a significant increase in the amounts of sphingomyelin and a decrease in phosphatidylglycerol. These changes were absent in PcAS mice and may be related to the altered re-uptake and synthesis of PL by injured cells or to PL contamination due to inflammatory cells. The plasma levels of PL and triacylglycerol (TG) were significantly higher in PbNK65 mice than in CTR or PcAS mice. Compared to PcAS or CTR mice in PbNK65 group all the PL classes were significantly increased with the exception of lisophosphatidilcholine (LisoPC) that was decreased. These plasma alterations may be related to an impaired activity of the enzymes involved in the lipoprotein metabolism during infections or inflammatory diseases. The most important observation, both in PbNK65 and PcAS mice, was the significant increase of docosahexahenoic acid (C22:6 n-3, DHA) compared to CTR, which was only partially reverted by DEX treatment, suggesting that the increase of DHA is not related to lung pathology but rather to the malaria infection. Analysis of the liver tissue of infected mice. The hypothesis that the higher PL and TG content of PbNK65 plasma might be due to an enhanced hepatic lipogenesis was confirmed by the higher TG and ChoE content of the liver of PbNK65 mice compared to PcAS and CTR. An increased ratio linoleic (LA)/arachidonic acid (AA) was also present possibly due to the impairment of the elongation/desaturation pathway from LA to AA acid. Higher levels of Hz, compared to PcAS, were present in PbNK65 mice and, in agreement with the Hz capability of stimulating Kupffer cells, we found higher levels of TNF-α. Both Hz and TNF-α can induce lipoperoxidation as confirmed by the elevated levels of malondialdehyde (MDA) in the liver of PbNK65 mice. This finding was paralleled by the lower content of glutathione and of antioxidant enzymes particularly in the late stage of the pathology. CONCLUSIONS This is the first time that a comprehensive analysis of the lipid content and inflammatory response of different organs in a model of murine MA-ARDS has been performed. All together the data suggest that in MA-ARDS as in other severe non infectious pathologies, a pulmonary-liver metabolic interplay exist which may contribute to the pathology. In PbNK65 mice, Hz and the derived inflammation play an important role in the lung pathology inducing changes in the lipid composition of lung and surfactant, cellular infiltration and cytokine production. Lung pathology is associated with liver disorders and alterations in the lipoprotein profile. Hz accumulation may induce macrophages to produce TNF-α and ROS that can interfere with liver functions by inducing lipogenesis and affecting the lipid profile of liver and plasma, which in turn contribute to the altered lipid composition of the lung tissue. These results confirm that severe malaria is a multi-organ dysfunction in which inflammation has an important role in different organs and thus, in addition to antimalarial treatment, adjunct therapies with anti-inflammatory drugs can be envisaged.
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Carpi, Mário Ferreira. « Efeito imediato e prolongado da administração precoce de óxido nítrico inalatório em crianças portadoras de síndrome do desconforto respiratório agudo / ». Botucatu : [s.n.], 2003. http://hdl.handle.net/11449/104678.

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Orientador: José Roberto Fioretto
Resumo: A Síndrome do Desconforto Respiratório Agudo (SDRA) é a forma clínica mais grave da lesão pulmonar aguda e, apesar do melhor entendimento de sua fisiopatologia, a taxa de mortalidade permanece elevada. O óxido nítrico inalatório (NOi) é um vasodilatador seletivo de áreas pulmonares ventiladas, promovendo a otimização da relação ventilação/perfusão nestas áreas, com melhora da oxigenação e facilitação do esvaziamento do ventrículo direito. Tais efeitos permitiriam a redução de parâmetros ventilatórios, habitualmente elevados na SDRA, diminuindo o risco de lesão pulmonar induzida pela ventilação mecânica e a morbi/mortalidade. O estudo teve como objetivos avaliar o efeito imediato e prolongado da administração precoce de NOi associada à terapia convencional sobre a oxigenação e parâmetros ventilatórios, mortalidade, tempo de internação na UTI Pediátrica e duração da ventilação mecânica em crianças portadoras de SDRA. Dois grupos de pacientes pediátricos com SDRA foram comparados: grupo NOi (GNO; n=18), seguido prospectivamente, composto de pacientes que receberam NOi associado à terapia convencional e grupo terapia convencional (GTC; n=21), avaliado retrospectivamente, formado de pacientes que utilizaram apenas terapia convencional. Os critérios para iniciar a administração do NOi foram: saturação arterial de oxigênio < 90% a despeito de uma fração inspirada de oxigênio (FiO2) 0,6 e de uma pressão expiratória final positiva (Peep) 10 cmH2O. A resposta imediata ao NOi foi avaliada em um teste de resposta de quatro horas, considerando resposta positiva um aumento na relação PaO2/FiO2 de 10 mmHg acima dos valores basais. A terapia convencional não foi modificada durante o teste. Nos dias subseqüentes os pacientes que exibiram resposta positiva continuaram recebendo a menor dose de NOi... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Acute respiratory distress syndrome (ARDS) is the most severe manifestation and the end spectrum of acute lung injury. It has been associated with high mortality rate, despite better understanding of its pathophysiology and recent therapeutic advances. Inhalde nitric oxide (iNO)-induced vasodilation of pulmonary vasculature adjacent to well-ventilated alveoli increases blood flow to these lung areas and preferentially shunt blood away from poorly ventilated regions, matching V/Q and reducing intrapulmonary shunt. This results in improved oxygenation and reduction of both pulmonary vascular resistence and right ventricle afterload. By improving V/Q matching, iNO may allow less aggressive mechanical ventilation (MV), which minimizes the risk of ventilator-induced lung injury and mortality. The aims of this study were: 1) to determine the acute and sustained effects of iNO on some oxygenation indexes and ventilator settings, to analyze the weaning process, and to assess the safety of NO inhalation; 2) to test the hypothesis that early administration of iNO would reduce mortality rate, intensive care length of stay, and the duration of MV comparing a group of pediatric ARDS patients treated with iNO plus conventional therapy with another treated only with conventional therapy. Children with ARDS, aged between one month and 12 years were studied. There were two groups: iNO group (iNOG; n=18) composed of patients prospectively enrolled from November 1998 to 2002, and conventional therapy group (CTG; n=21) consisting of historical control patients admitted from August 1996 to August 1998. Study groups were of similar ages, gender, primary diagnoses, pediatric risk of mortality score, and mean airway pressure. PaO2/FiO2 ratio was lower (CTG: 116.9l34.5; iNOG: 71.3l24.1 - p < 0.001) and oxygenation index higher (CTG: 15.2 (7.2-32.2); iNOG: 24.3 (16.3-70.4) - p < 0.001) in the iNOG. Therapy with iNO was introduced as early as 1.5 hours after ARDS.
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Sun, Xiaoguang, Biji Mathew, Saad Sammani, Jeffrey R. Jacobson et Joe G. N. Garcia. « Simvastatin-induced sphingosine 1−phosphate receptor 1 expression is KLF2-dependent in human lung endothelial cells ». SAGE PUBLICATIONS INC, 2017. http://hdl.handle.net/10150/623874.

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We have demonstrated that simvastatin and sphingosine 1-phosphate (S1P) both attenuate increased vascular permeability in preclinical models of acute respiratory distress syndrome. However, the underlying mechanisms remain unclear. As Kruppel-like factor 2 (KLF2) serves as a critical regulator for cellular stress response in endothelial cells (EC), we hypothesized that simvastatin enhances endothelial barrier function via increasing expression of the barrier-promoting S1P receptor, S1PR1, via a KLF2-dependent mechanism. S1PR1 luciferase reporter promoter activity in human lung artery EC (HPAEC) was tested after simvastatin (5 mu M), and S1PR1 and KLF2 protein expression detected by immunoblotting. In vivo, transcription and expression of S1PR1 and KLF2 in mice lungs were detected by microarray profiling and immunoblotting after exposure to simvastatin (10 mg/kg). Endothelial barrier function was measured by trans-endothelial electrical resistance with the S1PR1 agonist FTY720-(S)-phosphonate. Both S1PR1 and KLF2 gene expression (mRNA, protein) were significantly increased by simvastatin in vitro and in vivo. S1PR1 promoter activity was significantly increased by simvastatin (P < 0.05), which was significantly attenuated by KLF2 silencing (siRNA). Simvastatin induced KLF2 recruitment to the S1PR1 promoter, and consequently, significantly augmented the effects of the S1PR1 agonist on EC barrier enhancement (P < 0.05), which was significantly attenuated by KLF2 silencing (P < 0.05). These results suggest that simvastatin upregulates S1PR1 transcription and expression via the transcription factor KLF2, and consequently augments the effects of S1PR1 agonists on preserving vascular barrier integrity. These results may lead to novel combinatorial therapeutic strategies for lung inflammatory syndromes.
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