The Journal of surgical research
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The indications for immediate intubation in trauma are not controversial, but some patients who initially appear stable later deteriorate and require intubation. We postulated that initially stable, moderately injured trauma patients who experienced delayed intubation have higher mortality than those intubated earlier. ⋯ These findings suggest that delayed intubation is associated with increased mortality in moderately injured patients who are initially stable but later require intubation and can be predicted by the presence of rib fractures.
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Interleukin-6 (IL6) is a major inflammatory mediator and one of the first cytokines produced after traumatic brain injury (TBI). This study evaluates early behavioral changes and acute inflammation after TBI in IL6 knock-out mice using electromagnetic controlled cortical impact. ⋯ IL6 deficiency after TBI is associated with poor behavior performance, and appears to affect expression of IL1β and, possibly, HSP70.
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Renal ischemia/reperfusion (I/R) injury occurs in both native and transplanted kidneys. Hyperbaric oxygen (HBO) has been shown to prevent I/R injury in different tissues. The aim of this study was to evaluate the effect of HBO on renal I/R injury in rats. ⋯ Hyperbaric oxygen preconditioning (HBO-PC) can protect renal I/R injury against oxidative stress, and the up-regulation of HO-1 expression plays an essential role in HBO induced preconditioning effect.
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Acute coagulopathy of trauma (ACOT) has been described as a very early hypocoagulable state, but the mechanism remains controversial. One proposed mechanism is tissue hypoperfusion leading to protein C activation, with subsequent inhibition of Factors V and VIII. Variability in trauma has impeded the use of clinical data towards the elucidation of the mechanisms of ACOT, but thrombelastography (TEG) may provide insight by assessing hemostatic function from initial thrombin activation to fibrinolysis. We hypothesized that in a controlled animal model of trauma/hemorrhagic shock, clotting factor dysfunction is the predominant mechanism in early ACOT. ⋯ Clotting factor derangement leading to impaired thrombin generation is the principle etiology of ACOT in this model and not the dynamics of clot formation, fibrin cross-linking, clot strength/platelet function, or fibrinolysis.
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Substantial investigation has implicated mesenteric lymph as the mechanistic link between gut ischemia/reperfusion (I/R) and distant organ injury. Specifically, lymph diversion prevents acute lung injury (ALI) in vitro, and bioactive lipids and proteins isolated from postshock mesenteric lymph (PSML) maintain bioactivity in vitro. However, Koch's postulates remain to be satisfied via direct cross-transfusion into a naïve animal. We therefore hypothesized that real time cross-transfusion of postshock mesenteric lymph provokes acute lung injury. ⋯ Cross-transfusion of PSML into a naïve animal leads to PMN accumulation and provokes ALI. These data provide evidence that postshock agents released into mesenteric lymph are capable of provoking distant organ injury.