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 investigation of the trauma-induced innate immune responses is hampered by the wide variability in patients, type of trauma, and environmental factors. To circumvent this heterogeneity, we examined whether the systemic innate immune response toward human experimental endotoxemia is similar to the response during systemic inflammatory response syndrome after trauma. We tested the hypothesis that the innate immune response to pathogen-associated molecular pattern (e.g., lipopolysaccharides [LPSs]) and danger-associated molecular pattern (as induced by injury) leads to a comparable in vivo activation of human neutrophils. ⋯ A significant difference between both conditions was seen in CD66b expression and for endotoxin resulted in an increased CD66b expression, whereas injury did not. Neutrophil activation was present 3 h after onset of inflammation, both during experimental endotoxemia as well as in trauma patients. Endotoxin and trauma appear to induce a similar neutrophil activation phenotype.
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The aim of this study was to investigate the effect of 17β-estradiol (E2) on hepatocyte apoptosis after reduced-size hepatic ischemia/reperfusion (I/R) injury and its mechanism. A rat model of reduced-size hepatic I/R injury was established. Sprague-Dawley rats were randomly allocated into sham, I/R, and E2 + I/R group. 17β-Estradiol (4 mg/kg) or the vehicle was administered i.p. 1 h before ischemia and immediately after operation. ⋯ Furthermore, E2 inhibited hepatocellular apoptosis by upregulating the ratio of Bcl-2 and Bax expression, reduced cytosolic cytochrome c level, and decreased caspase 9 and caspase 3 activities. The 7-day survival rate was significantly higher in the E2 + I/R group than in the I/R group. These results indicated that E2 protects liver tissues from reduced-size hepatic I/R injury by suppressing mitochondrial apoptotic pathways.
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Polymorphonuclear granulocytes (PMNs) have been attributed a primarily deleterious role in the pathogenesis of acute lung injury (ALI). However, evidence exists that PMNs might also act beneficially in certain types of ALI. In this regard, we investigated the role of activated neutrophils in the pathophysiology of lung contusion-induced ALI. ⋯ In the presence of PMNs, BAL protein was further increased at 30 h when compared with the 3-h time point, which was not the case in the absence of PMNs. Taken together, in response to lung trauma, activated neutrophils control inflammation including mediator release from distant immune cells but simultaneously mediate pulmonary tissue damage. Thus, keeping in mind potential inflammatory adverse effects, modulation of neutrophil activation or trafficking might be a reasonable therapeutic approach in chest trauma-induced lung injury.
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The treatment of acute lung injury and septic complications after blunt chest trauma remains a challenge. Inhaled hydrogen sulfide (H₂S) may cause a hibernation-like metabolic state, which refers to an attenuated systemic inflammatory response. Therefore, we tested the hypothesis that inhaled H₂S-induced suspended animation may attenuate the inflammation after pulmonary contusion. ⋯ Furthermore, H₂S inhalation partially attenuated the mediator release in BAL and culture supernatants of Kupffer cells as well as splenic cells; it altered plasma cytokine concentrations but did not affect the trauma-induced changes in mononuclear cell culture supernatants. These findings indicate that inhaled H₂S induced a reduced metabolic expenditure and partially attenuated inflammation after trauma. Nevertheless, in contrast to hypoxic- or pathogen-induced lung injury, H₂S treatment appears to have no protective effect after blunt chest trauma.
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The transcutaneous partial pressure of oxygen (PtcO₂) index has been used to detect low-flow state in circulatory failure, but the value of the transcutaneous oxygen challenge test (OCT) to estimate low cardiac output has not been thoroughly evaluated. The prospective observational study examined 62 septic patients requiring PiCCO-Plus for cardiac output monitoring. Simultaneous basal blood gases from the arterial, central venous catheters were obtained. ⋯ The 10 OCT and the oxygen challenge index predicted a low CI (≤ 3 L/min per m) with an accuracy that was similar to central venous oxygen saturation, which was significantly better than the PtcO₂ index. For a 10 OCT value of 53 mmHg, sensitivity was 0.83; specificity, 0.86; a positive predictive value, 0.92; and a negative predictive value, 0.72 for detecting CI of 3 L/min per m or less. We propose that the OCT substituted for the PtcO₂ index as an accurate alternative method of PtcO₂ for revealing low CI in septic patients.