Effects of N-n-butyl haloperidol iodide on the hemodynamics and enzymes of myocardial tissue of myocardial ischemia-reperfusion injury in rabbits

AIM To evaluate the protective effect of N -n-butyl haloperidol iodide (F2) on myocardial ischemia-reperfusion injury, and to try to find the protective mechanism of F2. METHODS The myocardial ischemia-reperfusion injury animal model was established by ligaturing rabbit's left ventricular branch of coronary artery for 40 min and removing the ligationg later to reperfuse for 40 min in vivo . Different doses of F2 were administered by intravenous injection prior to the onset of ischemia. The changes of hemodynamics were recorded during the experiment, while those of superoxide dismutase (SOD), creatine kinase (CK), ATPase and the contents of malondiadehyde (MDA) of myocardial tissue were detected after reperfusion. RESULTS F2 could ameliorate the hemodynamics of ischemia-repefusion injured myocardium in a dose-dependent manner. The values of MAP, LVSP, ±d p /d t _ max were obviously higher than those of the ischemia-repefusion control group, while those of LVEDP were lower. F2 could also reduce the yield of MDA, protect the activities of SOD, Ca 2+ -ATPase, Na +,K +-ATPase, and minify the leakage of CK out of myocardial cells in a dose-dependent manner. CONCLUSION F2 could exert an apparently protective effect against myocardial ischemia-reperfusion injury.