Objective: To investigate the changes in heart function and myocardial mechanics in murine sepsis model, and the mechanism of the protective effect of dexamethasone on heart.
Methods: Wistar rats were randomly divided into control group, lipopolysaccharide (LPS) group (4 mg/kg LPS intravenously), LPS+dexamethasone group (4 mg/kg LPS+2 mg/kg dexamethasone intravenously), with 32 rats in each group. A catheter was passed through right common carotid artery to the left cardiac ventricle. Function of the left ventricle was monitored, and blood was drawn at 0, 2, 4, 6 hours to detect concentrations of tumor necrosis factor-alpha (TNF-alpha), troponin T (TnT), with 8 rats for each time point.
Results: In sepsis rats, TnT increased significantly and could be lowered by dexamethasone [at 6 hours after the treatment (1.76+/-0.57) microg/L vs. (0.70+/-0.36) microg/L, P<0.01]. There were changes in left ventricular peak systolic pressure (LVPP) and maximum rate of intraventricular pressure rise/down (+/-dp/dt max) to certain extent, and increase in left ventricular end-diastolic pressure (LVEDP), but these changes could be ameliorated by using dexamethasone. TNF-alpha increased significantly in sepsis rats, but dexamethasone could lower its level [at 2 hours after the treatment (11.22+/-2.38) pmol/L vs. (7.62+/-3.21) pmol/L, P<0.01].
Conclusion: Myocardium is remarkably damaged in rats with sepsis. TNF-alpha could be regarded as one of the factors which could produce injury to myocardium. Dexamethasone could alleviate cardiac damage produced by endotoxin in sepsis model.