The Journal of surgical research
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Although hyperglycemia has been associated with poor postoperative outcomes, preoperative hyperglycemia is not used as a screening tool in patients without diabetes. We evaluated preoperative glucose as a marker for postoperative outcomes in patients without diabetes to assess its usefulness as a potential screening tool. ⋯ In patients without known diabetes, preoperative glucose is a significant marker for postoperative complications even at moderate levels of hyperglycemia. Some of these patients likely had prediabetes or unrecognized diabetes at the time of surgery. Further studies are needed to determine whether such screening and follow-up of preoperative hyperglycemia in all patients would be effective in lowering complication rates.
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The renin-angiotensin system (RAS) affects inflammatory responses during sepsis. Nonproteolytic activation of prorenin by the (pro)renin receptor has recently been shown to stimulate the tissue RAS. In the present study, the effect of (pro)renin receptor blocker (PRRB) pretreatment on sepsis in a rat cecal ligation and puncture (CLP) model was investigated. ⋯ PRRB significantly improved the survival rate of rats with clinically relevant sepsis, possibly by attenuating a sepsis-induced systemic inflammatory response. We propose that overactivation of the RAS by activation of prorenin in foam cells may be a significant contributor to sepsis.
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Dexmedetomidine (DEX) has been shown to decrease ischemia-reperfusion (I/R) injury in kidney and brain tissues. In this study, the effects of DEX were evaluated in skeletal muscle during I/R injury. ⋯ We found that DEX exhibits protective effects against skeletal muscle I/R injury. These results underscore the necessity of human studies with DEX to determine if it is beneficial for preventing skeletal muscle I/R injury.
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ischemic preconditioning (IPC) protects against liver ischemia-reperfusion (IR) injury. The mechanism involves nitric oxide metabolism but the importance of endothelial nitric oxide synthase (eNOS) has not been established. Heme oxygenase-1 (HO-1) protects against liver IR but it is unclear if this depends on nitric oxide synthase. ⋯ This study developed and used an eNOS-/- model to demonstrate that eNOS mediates protection against liver IR injury by IPC. The eNOS expression and activity and HO-1 expression are increased independently in liver IPC and IR, with HO-1 expression increased in the later stages of IPC and IR.