Etomidate alleviates cardiac dysfunction, fibrosis and oxidative stress in rats with myocardial ischemic reperfusion injury.

BACKGROUND

Etomidate has been shown to reduce ischemia/reperfusion (I/R) injury in several tissues. Here we aimed to investigate the protective effects of etomidate on I/R injury in Sprague-Dawley (SD) rats.

METHODS

Thirty rats were randomly divided into 5 groups and pretreated with saline or 0.5/1/2 mg/kg etomidate. I/R injury was induced in all groups except the sham control group. After administration with saline or 0.5/1/2 mg/kg etomidate daily for another 27 days, rats were sacrificed and the effects of etomidate were analyzed.

RESULTS

Treatment with etomidate dose dependently improved echocardiography indexes, ameliorated myocardial histological alterations and reduced serum creatine kinase isoenzyme (CK-MB), myoglobin (Mb) and troponin I (cTnl) levels. Fibrosis markers transforming growth factor beta (TGF-β), alpha-smooth muscle actin (α-SMA) and fibronectin was decreased with etomidate treatment. Etomidate also decreased oxidative stress and inflammation in rats, indicated by increased superoxide dismutase (SOD) and glutathione (GSH), and reduced malondialdehyde (MDA) in myocardial tissues, as well as decreased inducible NO synthase (iNOS) and increased interleukin (IL)-10 in both serum and myocardial tissues.

CONCLUSIONS

Altogether, we showed that etomidate alleviated I/R injury in rats through reduced cardiac dysfunction, fibrosis and oxidative stress. These results supported the protective role of etomidate to myocardial I/R injury.