The Journal of surgical research
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Acute traumatic injury is a complex disease that has remained a leading cause of death, which affects all ages in our society. Direct mechanical insult to tissues may result in physiological and immunologic disturbances brought about by blood loss, coagulopathy, as well as ischemia and reperfusion insults. This inappropriate response leads to an abnormal release of endogenous mediators of inflammation that synergistically contribute to the incidence of morbidity and mortality. ⋯ The enigmatic immunopathology of the human immunologic response after severe trauma, however, has never more been apparent and there grows a need for a clinically relevant animal model, which mimics this immune physiology to enhance the care of the most severely injured. This has necessitated preclinical studies in a more closely related model system, the nonhuman primate. In this review article, we summarize animal models of trauma that have provided insight into the clinical response and understanding of cellular mechanisms involved in the onset and progression of ischemia-reperfusion injury as well as describe future treatment options using immunomodulation-based strategies.
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The incidence of splenectomy after trauma is institutionally dependent and varies from 18% to as much as 40%. This is important because variation in management influences splenic salvage. The aim of this study was to investigate whether differences exist between Dutch level 1 trauma centers with respect to the treatment of these injuries, and if variation in treatment was related to splenic salvage, spleen-related reinterventions, and mortality. ⋯ Although observation rates were comparable among the academic trauma centers, embolization and surgery rates varied. A nearly 5-fold increase in the odds of operative management was observed in one hospital, and another hospital had significantly lower odds of splenic salvage. The development of a national guideline is recommended to minimalize splenectomy after trauma.
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Mortality in sepsis is most often attributed to the development of multiple organ failure. In sepsis, inflammation-mediated endothelial activation, defined as a proinflammatory and procoagulant state of the endothelial cells, has been associated with severity of disease. Thus, the objective of this study was to test the hypothesis that adenosine monophosphate-activated protein kinase (AMPK) activation limits inflammation and endothelium activation to protect against organ injury in sepsis. 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), which is an adenosine monophosphate analog, has been used to upregulate activity of AMPK. Compound C is a cell-permeable pyrrazolopyrimidine compound that inhibits AMPK activity. ⋯ In this model, activation of AMPK was protective, and AICAR minimized organ injury by decreasing inflammatory cytokines and endothelial activation. These data suggest that AMPK signaling influences sepsis or LPS-induced endothelial activation and organ injury.
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The purpose of this study was to assess the direct and indirect relationships between first-case tardiness (or "late start"), turnover time, underused operating room (OR) time, and raw utilization, as well as to determine which indicator had the most negative impact on OR utilization to identify improvement potential. Furthermore, we studied the indirect relationships of the three indicators of "nonoperative" time on OR utilization, to recognize possible "trickle down" effects during the day. ⋯ The study findings clearly suggest that OR utilization can be improved by focusing on the reduction of underused OR time at the end of the day. Improving the prediction of total procedure time, improving OR scheduling by, for example, altering the sequencing of operations, changing patient cancellation policies, and flexible staffing of ORs adjusted to patient needs, are means to reduce "nonoperative" time.
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Postoperative cognitive dysfunction is increasingly recognized as an important clinical syndrome. Inhalation anesthetics are commonly used during surgery, and it has been proposed that inhalation anesthetics impair cognitive function. However, there are few clinical interventions and treatments available to prevent this disorder. GTS-21, a selective agonist of alpha 7 nicotinic acetylcholine receptor, has been indicated to exert neuroprotective effects in the experimental animal models of neurodegenerative diseases. Therefore, we hypothesized that pretreatment with GTS-21 attenuates isoflurane-induced cognitive decline in aged rats. ⋯ The study demonstrated that pretreatment with α7 nicotinic acetylcholine receptor agonist GTS-21 attenuates isoflurane-induced learning and memory impairment in aged rats.