Protective effects of dexamethasone on myocardium in rats with sepsis

Objective To investigate th e changes in heart function and myocardial mechanics in murine sepsis model, and t he mechanism of the protective effect of dexamethasone on heart. Methods Wistar rats were randomly divided into control group, lipopolysaccharide (LPS) g roup (4 mg/kg LPS intravenously), LPS+dexamethasone group (4 mg/kg LPS+2 mg/kg d examethasone intravenously), with 32 rats in each group. A catheter was passed t hrough right common carotid artery to the left cardiac ventricle. Function of th e left ventricle was monitored, and blood was drawn at 0, 2, 4, 6 hours to detec t concentrations of tumor necrosis factorα (TNFα), tro ponine T (TnT), with 8 rats for each time point. Results In sepsis rats, TnT increased significantly and could be lowered by dexamethaso ne 〔at 6 hours after the treatment (1.76±0.57) μg/L vs. (0.70±0.36 ) μg/L, P0.01〕. There were c hanges in left ventricular peak systolic pessure (LVPP) and maximum rate of intr aventricular pressure rise/down (±dp/dt max) to certain extent, and increase in l eft ventricular end-diastolic pressure (LVEDP), but these changes could be ameliorated by using dexamethasone. TNFα increased signif icantly in sepsis rats, but dexamethasone could lower its level 〔at 2 hours aft er the treatment (11.22±2.38) pmol/L vs. (7.62±3.21) pmol/L, P0.0 1〕. Conclusion Myocardium is remarkably damaged in rats with sepsis. TNFα could be regarded as one of the factors which could produce injury to myocardium. Dexame thasone could alleviate cardiac damage produced by endotoxin in sepsis model .