The Journal of surgical research
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Comparative Study Observational Study
Fibrinogen in trauma, an evaluation of thrombelastography and rotational thromboelastometry fibrinogen assays.
Identifying hypofibrinogenemia in trauma is important. The optimal method of fibrinogen determination is unknown. We therefore evaluated fibrinogen levels determined by two whole blood viscoelastic hemostatic assays, thrombelastography functional fibrinogen (FF) and rotational thromboelastometry FIBTEM in trauma patients and compared these with the plasma-based Clauss method. ⋯ The viscoelastic hemostatic assays for determining fibrinogen levels, FIBTEM and FF, are both correlated with the Clauss fibrinogen level, and there are no differences in the strength of these correlations. In this study, specific fibrinogen levels at arrival to the emergency department were indicative, although not necessarily causal, of increased odds of receiving a transfusion.
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Sepsis is characterized as a systemic inflammatory response syndrome during infection, which can result in multiple organ dysfunction and death. Ursolic acid (UA), a pentacyclic triterpene acid, has been reported to have potent anti-inflammatory and antioxidant properties. The aim of this study was to detect the possible protective effects of UA on sepsis-evoked acute lung injury. ⋯ These findings indicate that UA exerts protective effects on CLP-induced septic rats. UA may be a potential therapeutic agent against sepsis.
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Observational Study
Ultrasonographic evaluation of abdominal organs after cardiac surgery.
Disturbances of the hepatosplanchnic region may occur after cardiac operations. Experimental studies have implicated impairment of splanchnic blood supply in major abdominal organ dysfunction after cardiopulmonary bypass (CPB). We investigated the impact of the cardiac operation and CPB on liver, kidney, and renal perfusion and function by means of ultrasonography and biochemical indices in a selected group of cardiac surgery patients. ⋯ The increase in portal vein flow and velocity and the decrease in hepatic artery flow and velocity in the period after CPB might be attributed to the hypothermic bypass technique and the hepatic arterial buffer response, respectively. The decrease in renal blood flow and velocity and the parallel increase in Doppler renal pulsatility index and renal resistive index could be considered as markers of kidney hypoperfusion and intrarenal vasoconstriction. Maintaining a high index of suspicion for the early diagnosis of noncardiac complications in the period after CPB and institution of supportive care in case of compromised splanchnic perfusion are warranted.
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Lipopolysaccharide (LPS) has a deleterious effect on several organs, including the liver, and eventually leads to endotoxic shock and death. LPS-induced hepatotoxicity is characterized by disturbed intracellular redox balance and excessive reactive oxygen species (ROS) accumulation, leading to liver injury. We have shown that treatment with suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor, improves survival in a murine model of LPS-induced shock, but the protective effect of SAHA against liver damage remains unknown. The goal of this study was to investigate the mechanism underlying SAHA action in murine livers. ⋯ Our data indicate, for the first time, that SAHA is capable of alleviating LPS-induced hepatotoxicity and suggest that a blockade of the upstream events required for apoptosis signal-regulating kinase-1 action may serve as a new therapeutic option in the treatment of LPS-induced inflammatory conditions.
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Ketamine, a noncompetitive N-methyl-D-aspartate receptor antagonist, is widely used as an intravenous anesthetic agent and has also been shown to possess anti-inflammatory effects, but its effects on high-mobility group box-1 (HMGB1) have not been well defined. In the present study, we investigated the effects of ketamine on HMGB1 in lipopolysaccharide (LPS)-induced Raw264.7 cells and in a mouse model of cecal ligation and puncture-induced sepsis. ⋯ Ketamine inhibits LPS-induced HMGB1 release through HO-1 induction, and these effects may be mediated by blockade of p38 MAPK and Nrf2 signaling pathways.