The effect of isosorbide dinitrate on cardiac function after cardiopulmonary resuscitation in a porcine model / 中华急诊医学杂志

ABSTRACT

Objective To assess the effect of isosorbide dinitrate on the improvement of cardiac function after cardiopulmonary resuscitation (CPR) by regulating myocardial cells apoptosis..Methods Total of 30 domestic pigs were divided into three groups randomly (random mumber) after anesthetizationthe sham group (n=6),the control group (n=12),and the isosorbide dinitrate group (n=12).Cardiac arrest of ventricular fibrillation was induced by programed electrical stimulation in the control and isosorbide dinitrate groups.Isosorbide dinitrate was infused at the rate of 2 μg/(kg·min) in the isosorbide dinitrate group.Coronary perfusion pressure (CPP) and cardiac output (CO) were recorded at baseline,2,6,12 and 24 h after restoration of spontaneous circulation (ROSC).Myocardial enzyme and heart fatty acid binding protein (H-FABP) was tested at the same time points.At 24 h after ROSC,the animals were sacrificed to obtain the myocardium for pathological section and Western blot.The expression of Bcl-2,Bax and activated Caspase-3 were tested and apoptosis was tested by TUNEL and apoptosis index was calculated.Results Right atrial pressure (RAP) increased after ROSC and decreased in the isosorbide dinitrate group compared with the control group (P＜0.05).CPP at 12,24 h after ROSC and CO at 24 h after ROSC in the isosorbide dinitrate group increased significantly compared with the control group (both P＜0.05).HE staining revealed that the injury of myocardial cells was ameliorated in the isosorbide dinitrate group.Apoptosis index of the isosorbide dinitrate group significantly decreased than the control group [(37.8±15.5)％ vs (13.1±0.5)％,P＜0.05].The expression of Bax and activated Caspase-3 decreased while Bcl-2 and Bcl-2/Bax increased after ROSC in the isosorbide dinitrate group compared with the control group (all P＜0.05).Conclusions Isosorbide dinitrate could improve the isehemia/reperfusion injury and cardiac function after ROSC by inhibiting apoptosis regulated with Caspase-3 pathway.