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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Few studies were performed to investigate the association between tissue Doppler imaging parameters about left ventricular (LV) systolic function and LV systolic asynchrony and prognosis in patients with septic shock and normal LV ejection fraction (LVEF). This prospective study was performed from January 2010 to April 2012 in a medical intensive care unit. Fifty-one patients with septic shock and LVEF greater than or equal to 50% were analyzed. ⋯ The patients with Sm-mean greater than or equal to 6.2 cm/s or Ts-SD less than 33 ms had higher 28-day mortality. In the Cox multivariate analysis, Sm-mean, Ts-SD, and mean arterial blood pressure emerged as independent predictors for 28-day mortality. We concluded that LV systolic dysfunction and systolic asynchrony assessed by tissue Doppler imaging were associated with improved 28-day all-cause mortality in patients with septic shock and normal LVEF.
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S100A12 is highly expressed, and serum levels correlate with individual disease activity in patients with inflammatory diseases. We here sought to determine the extent of S100A12 release and its soluble high-affinity receptor for advanced glycation end products (sRAGE) in patients with severe sepsis stratified to the three most common infectious sources (lungs, abdomen, and urinary tract) and to determine S100A12 and sRAGE concentrations at the site of infection during peritonitis. Two patient populations were studied: (a) 51 patients with sepsis due to (i) peritonitis (n = 12), (ii) pneumonia (n = 29), or (iii) urinary tract infection (n = 10); and (b) 17 patients with peritonitis. ⋯ In conclusion, in severe sepsis, S100A12 is released systemically irrespective of the primary source of infection. During abdominal sepsis, S100A12 release likely predominantly occurs at the site of infection. Concentrations of its high-affinity sRAGE do not change during infection or human endotoxemia.
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Once established, the acute respiratory distress syndrome (ARDS) is highly resistant to treatment and retains a high mortality. We hypothesized that preemptive application of airway pressure release ventilation (APRV) in a rat model of trauma/hemorrhagic shock (T/HS) would prevent ARDS. ⋯ Our findings demonstrate that preemptive mechanical ventilation with APRV attenuates the clinical and histologic lung injury associated with T/HS. The mechanism of injury prevention is related to preservation of alveolar epithelial and endothelial integrity. These data support our hypothesis that preemptive APRV, applied using published guidelines, can prevent the development of ARDS.
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No drug therapy has demonstrated improved survival following cardiac arrest (CA) of cardiac or noncardiac origin. In an effort to translate the cardiorescue properties of Adenocaine (adenosine and lidocaine) and magnesium sulfate (ALM) from cardiac surgery and hemorrhagic shock to resuscitation, we examined the effect of ALM on hemodynamic rescue and coagulopathy following asphyxial-induced CA in the rat. ⋯ Small bolus of 0.9% NaCl ALM improved survival and hemodynamics following nonhemorrhagic, asphyxial CA and corrected prolonged clot times and clot retraction compared with controls.
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It has been shown that the innate immune system mediates acute lung inflammation triggered by intestinal trauma. Sexual dimorphism modulates the profile of TH1 and TH2 lymphocytes, and accordingly sex hormones may modulate acute lung inflammation by intestinal ischemia/reperfusion (I/R). Studies indicate that female rats are relatively resistant to organ injury caused by hemorrhagic shock and that the gut of female is more resistant than that of the male to deleterious effects of ischemic injury. At the present study, we investigated the effect of estradiol (E(2)) on the lung inflammation after intestinal I/R and its interaction with the nitric oxide (NO) pathway. ⋯ Estradiol treatment is able to reduce lung inflammation due to intestinal I/R, but with the concomitant blockade of NOS activity, this effect is abolished. Nitric oxide probably reduces the vascular deleterious effects of intestinal I/R, and E(2) pretreatment reduces lung inflammation after intestinal I/R and exerts these effects by modulating eNOS protein expression in the lungs.