【摘要】 目的：研究中药有效成分黄芩苷（baicalin）对大鼠心肌缺血再灌注损伤的作用及其机制。方法：雄性Wistar大鼠随机分为4组,假手术组、对照组和黄芩苷50,100 mg·kg^-1组。结扎大鼠左冠状动脉前降支30 min后松开结扎线120 min复制心肌缺血-再灌注损伤模型,以多道生理记录仪持续记录左室压力变化速率(±dp/ dt_max)和左室舒张末期压（LVEDP）的变化。检测心肌丙二醛（MDA）含量、超氧化物歧化酶（SOD）、Na⁺-K⁺-ATP酶和Ca²⁺-ATP酶活性以及血清乳酸脱氢酶（LDH）和磷酸肌酸激酶（CK）含量,以透射电镜观察心肌超微结构的改变。结果：与假手术组比较,对照组大鼠左室±dp/dt_max明显降低（P＜0.01）,而LVEDP明显升高（P＜0.01）。静脉注射黄芩苷50,100 mg·kg^-1可使降低的±dp/dt_max明显升高（P＜0.05,P＜0.01）,升高的LVEDP显著降低（P＜0.05,P＜0.01）。黄芩苷组血清CK和LDH含量分别是（72±19）kU·L^-1,（64±15）kU·L^-1和（1 365±209）U·L^-1,（1 124±169）U·L^-1,均明显低于对照组[（90±23）U·L^-1和（1 826±123）U·L^-1,P＜0.01]。对照组大鼠心肌SOD,Na⁺-K⁺-ATP酶和Ca²⁺-ATP酶活性均明显低于假手术组,而降低的酶活性可被预先给予黄芩苷所升高（P＜0.05,P＜0.01）。此外,黄芩苷还可降低缺血心肌MDA含量,改善心肌超微结构。结论：黄芩苷通过清除氧自由基,抗脂质过氧化,改善心肌ATP酶活性而保护心肌缺血再灌注损伤。更多还原

【Abstract】 AIM:To study the protective effects of baicalin on myocardial ischemia-reperfusion injury in rats.METHODS:The models of myocardial ischemia-reperfusion injury were established by occluding left anterior descending coronary artery（LAD）for 30 min,followed by reperfusion for 120 min.The rate of rise and decline of left ventricular pressure(±dp/dt_max)and end-diastolic pressure of left ventricle（LVEDP）were monitored continuously with polygraph.After reperfusion,the blood and myocardium samples were taken for determination of malondialdehyde（MDA）content,superoxide dismutase（SOD）,Na⁺-K⁺-ATPase,Ca²⁺-ATPase activities in myocardium,creatine kinase（CK）and lactate dehydrogenase（LDH）in serum with spectrophotometer.The uhrastruetural changes in ischemic myocardium were assessed by transmission electron microscope.RESULTS: Compared with control group,baicalin treatment with 50 mg·kg^-1 and 100 mg·kg^-1 depressed the changes in±dp/ dt_max and LVEDP,decreased plasma CK and LDH levels,reduced myocardial MDA content,and increased the activit- ies of SOD,Na⁺-K⁺-ATPase,and Ca²⁺-ATPase in myocardium following ischemia-reperfusion.The ultrastructural injury in reperfused myocardium was relieved.CONCLUSION:Baicalin possesses a protective effect against my- ocardial isehnemia-reperfusion injury through scavenging oxide radicals and improving Na⁺-K⁺-ATPase and Ca²⁺- ATPase activities.更多还原