卡维地洛对大鼠急性缺血再灌注损伤的心肌保护作用研究

 目的研究卡维地洛对大鼠心肌缺血再灌注损伤的保护作用及其作用机制。方法将大鼠随机分为假手术(sham)组、缺血再灌注(IRI)组、卡维地洛(CVD)组。结扎左冠状动脉前降支致缺血30min后复灌4h,制作心肌缺血再灌注损伤模型。于再灌4h末测定左室收缩压(LVP)、左室舒张末压(LVEDP)、左室发展压(LVDP=LVP-LVEDP)、左室最大收缩及舒张速度(±dp/dt);测定血液中肌酸磷酸激酶(CK)、乳酸脱氢酶(LDH)及丙二醛(MDA)和超氧化物歧化酶(SOD)含量以及心肌梗死范围。结果与假手术组相比,IRI组LVP,LVDP,±dp/dt及SOD降低,LVEDP,CK,LDH及MDA均升高,伴梗死范围扩大(P<0.01);与IRI比较,CVD组LVP,LVDP,±dp/dt及SOD升高,LVEDP,CK,LDH及MDA均降低,伴梗死范围缩小(P<0.01)。结论卡维地洛具有防止心肌再灌注损伤的作用,该作用与其β受体阻断和抗氧化有关。

Protective effects of carvedilol on myocardial ischemia and reperfusion injury in rat

OBJECTIVE To examine the effects and the mechanism of carvedilol on myocardial ischemia and reperfusion injury. METHODS Rats were divided randomly into three groups, sham operation group(sham), myocardial ishemia and reperfusion group (IRI) and carvedilol group(CVD). The left anterior descending branch of coronary artery was ligated for 30 minutes and reperfused for 4 h to build the myocardial ischemia and reperfusion injury model. After 4 h reperfusion, the hemodynamic parameter, such as left ventricular peak pressure(LVP), left ventricular end diastolic pressure (LVEDP), left ventricular developed pressure(LVDP=LVP-LVEDP) and peak systolic or diastolic velocity(+dp/dt), were measured. The activity of creatine phosphokinase(CK), lactate dehydrogenase(LDH), and superoxide dismutase(SOD), the content of malondialdehyde(MDA) and the infarct size were investigated too. RESULTS Compared with sham group, LVP, LVDP and ±dp/dt and SOD decreaed, and LVEDP, CK, LDH and MDA decreased, increaed, infarct size increaed in IRI group. Compared with IRI group, LVP, LVDP and ±dp/dt and SOD incresed, LVEDP, CK, LDH and MDA decreased infarct size was reduced in CVD group. CONCLUSION Carvedilol relieves the isehemia-reperfusion injury and the cardioprotection may be due to its β-recepfor block and antioxidant effects.