摘要
采用Langendorff离体大鼠心脏灌流模型,研究了小檗胺(BA)对心肌缺血—再灌注损伤的保护作用。离体心脏全心缺血40min后再灌注时,心功能明显低下,发生严重心律失常及心肌组织内超氧化物歧化酶(SOD)活性明显下降(从对照组的102.7±10.0μg/g下降到76.8±10.5μg/g,P<0.01)。BA 1μmol/L明显促进再灌注后冠脉流量(P<0.05)和心肌收缩幅度(P<0.01)的恢复,并抑制静息张力的升高(P<0.01).此外,BA还能有效地阻止心室颤动的发生,防止心肌SOD活性下降(P<0.01)。我们推测BA是通过清除自由基和保护SOD活性而起到抗再灌注损伤作用的。我们的结果表明,BA能对抗心肌缺血一再灌注损伤。
The protective effects of berbamine (BA) against ischemia/reperfusion injury were studied in Langendorff perfused rat hearts. Depressed heart function, severe arrhythmias and decreased SOD activity(from control value 102.7±10.0μg/g to 76.8±10.5μg/g, P<0.01) occurred during reperfusion after global ischemia for 40 minutes. BA 1 μmol/L apparently improved the recovery of coronary flow (P<0.05) and contraction am plitude (p<0.01), and inhibited the rise of resting tension (p<0.01) during reperfusion. Moreover, BA could abolish ventricular fibrillation and prevent the dacrease in myocardial SOD activity (p<0.01) induced by reperfusion. We infer that BA attenuates reperfuaion injury probably by directly scavenging free radicals and preserving SOD activity in the myocardium. Our resuha show that BA can protect the myocardium against ischemia/reperfusion injury.
出处
《中国循环杂志》
CSCD
1991年第3期227-229,共3页
Chinese Circulation Journal
关键词
小檗胺
再灌注损伤
心肌缺血
药理
Berbamine
Ischemia/reperfusion injury
Free radical scavengers
