Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Mortality in ST-elevation myocardial infarction (STEMI) patients developing cardiogenic shock (CS) during hospitalization is high. Catecholamines, ischemia, and inflammation (parameters present in CS) affect the endothelium. We hypothesized that plasma level of biomarkers reflecting endothelial damage would be associated with CS and mortality. ⋯ Patients with suspected STEMI patients and admission-CS/cath.lab.-CS had elevated admission levels of sTM and Syndecan-1 compared with no CS patients. Patients developing late CS had higher sTM plasma concentration compared with patients without shock. However, the biomarker levels were not independently associated with late CS and mortality.
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Brain death is associated with significant lung injury and inflammation. This has been associated with worse long-term outcomes for transplanted lungs. Direct peritoneal resuscitation (DPR) reduces systemic inflammation in brain death and improves lung procurement rate. The effect of DPR on macrophage and neutrophil infiltration in the lungs is not known. ⋯ Animals that received TIVF alone had significant increases in inflammatory cytokines within the lung tissue, leading to adhesion molecule expression and ultimately leukocyte infiltration. Each stage of inflammation was affected by DPR. Using DPR in brain dead organ donors shows promise as a way to reduce lung injury and inflammation.
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Angiotensin II plays a vital role in the pathogenesis of acute respiratory distress syndrome (ARDS). However, its mechanism is not well defined. Angiotensin II upregulates the expression of soluble epoxide hydrolase (sEH; Ephx2). sEH is suggested as a potential pharmacologic target for ARDS. The present study investigates whether the sEH is involved in the angiotensin II-triggered pulmonary inflammation and edema using an angiotensin II-induced lung injury animal model. ⋯ Angiotensin II-induced lung injury was improved in sEH gene deleted mice. The angiotensin II-triggered pulmonary inflammation is mediated, at least in part, through the sEH.
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Acute lung injury (ALI) and its severe form, acute respiratory distress syndrome, remain the leading causes of morbidity and mortality in intensive care units. Ulinastatin (UTI), a serine protease inhibitor, possesses anti-inflammatory properties and has been suggested to modulate lipopolysaccharide (LPS)-induced sepsis; thus, it is now widely used in the treatment of pancreatitis, sepsis, and septic shock. Toll-like receptor 4 (TLR4), an essential LPS signaling receptor, plays a critical role in the activation of innate immunity. ⋯ Furthermore, UTI significantly attenuated LPS-induced increases in TLR4 protein expression and NF-κB activation in lung tissues. Similarly, UTI markedly attenuated TLR4 expression and NF-κB activation in LPS-stimulated BEAS-2B cells. These findings indicate that UTI ameliorates LPS-induced ALI by attenuating the TLR4/NF-κB pathway activation.
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Severe sepsis and septic shock are the biggest cause of mortality in critically ill patients. Obesity today is one of the world's greatest health challenges. Little is known about the extent of involvement of the white adipose tissue (WAT) in sepsis and how it is being modified by obesity. ⋯ Nonobese septic mice have an increase in mitochondrial density compared with obese septic mice. Furthermore, nonobese septic mice have an increase in uncoupling protein-1 expression. Although the WAT of nonobese mice have multiple changes characteristic of browning during sepsis, these changes are markedly blunted in obesity.