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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The objective of this study was to determine the effects of a TREM (triggering receptor expressed on myeloid cells 1)-like transcript 1-derived peptide (LR12) administration during septic shock in pigs. Two hours after induction of a fecal peritonitis, anesthetized and mechanically ventilated adult male minipigs were randomized to receive LR12 (n = 6) or its vehicle alone (normal saline, n = 5). Two animals were operated and instrumented without the induction of peritonitis and served as controls (sham). ⋯ These disorders were largely attenuated by LR12. In particular, cardiovascular failure was dampened as attested by a better mean arterial pressure, cardiac index, cardiac power index, and S(v)O(2), despite lower norepinephrine requirements. LR12, a TREM-like transcript 1-derived peptide, exhibits salutary properties during septic shock in adult minipigs.
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Our objectives were to determine the incidence of critical illness-related corticosteroid insufficiency (CIRCI) in patients with septic shock using a 1 μg corticotropin (ACTH) test and to describe their clinical outcomes. We retrospectively identified 219 consecutive patients with septic shock assessed for CIRCI with a 1 μg ACTH test. Standardized testing involved plasma cortisol measurements at baseline (T0) and at 30 min (T30) and 60 min (T60) after ACTH administration. ⋯ The incidence of CIRCI based on 1 μg ACTH was high in this septic shock cohort. The highest mortality rates were observed in patients with high baseline cortisol and in those who failed to respond appropriately to ACTH. The administration of corticosteroids was not associated with a reduction in mortality.
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Gastrointestinal bacteria and epithelia contribute to systemic inflammation and infections in critically ill patients, but the gut microbiota in these diseases has not been analyzed dynamically by molecular fingerprinting methods. This study aimed to identify ileal flora dysbiosis pattern and bacterial species that changed significantly in a rat model of intestinal ischemia and reperfusion and illustrate time courses of both epithelial alterations and gut flora variations in the same injury. Forty-eight rats were randomized into eight groups (n = 6/group). ⋯ The specific dysbiosis were characterized by Escherichia coli proliferation and Lachnospiraceae and Lactobacilli reduction. These bacteria that contributed most were identified by principal component analysis and sequencing and confirmed by real-time polymerase chain reaction. In addition, alterations of ileal microbiota followed epithelial changes in the time course of reperfusion.
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Systemic inflammatory response syndrome (SIRS) is a fundamental host response common to bacterial infection and sterile tissue injury. Systemic inflammatory response syndrome can cause organ dysfunction and death, but its mechanisms are incompletely understood. Moreover, SIRS can progress to organ failure or death despite being sterile or after control of the inciting infection. ⋯ Critically, activated protein C pretreatment (n = 4) allowed mtDNA levels to decay after bacterial clearance with sparing of organ function and survival. In summary, host tissue injury correlates with mtDNA whether infective or sterile. Mitochondrial DNA and bDNA polymerase chain reactions can quantify tissue injury incurred by septic or sterile mechanisms and suggest the source of SIRS of unknown origin.
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Cholecystokinin (CCK) was first described as a gastrointestinal hormone, but its receptors have been located in cardiac and vascular tissues, as well as in immune cells. Our aims were to investigate the role of CCK on lipopolysaccharide (LPS)-induced hypotension and its ability to modulate previously reported inflammatory mediators, therefore affecting cardiovascular function. To conduct these experiments, rats had their jugular vein cannulated for drug administration, and also, the femoral artery cannulated for mean arterial pressure (MAP) and heart rate records. ⋯ Physiological CCK concentration reduced nitrite and iNOS synthesis by peritoneal macrophages, possibly through a self-regulatory IL-10-dependent mechanism. Together, these data suggest a new role for the peptide CCK in modulating MAP, possibly controlling the inflammatory response, stimulating the anti-inflammatory cytokine, IL-10, and reducing vascular and macrophage iNOS-derived nitric oxide production. Based on these findings, CCK could be used as an adjuvant therapeutic agent to improve cardiovascular function.