冠心康对大鼠缺血心肌细胞ATP敏感钾通道的影响

作者	单位
张娜	上海中医药大学附属龙华医院
陈富荣	上海中医药大学附属龙华医院
章怡祎	上海中医药大学附属龙华医院
刘萍	上海中医药大学附属龙华医院

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中文摘要:

目的观察中药复方冠心康对大鼠缺血心肌细胞ATP敏感钾(ATP-sensitive potassium channel,KATP)通道的影响,进一步探讨冠心康保护心血管、抗心肌缺血可能的作用机制。方法随机选取Wistar大鼠分为正常组、模拟缺血再灌注损伤模型组、模型加格列苯脲组、模型加吡那地尔组、模型加冠心康组、模型加冠心康加格列苯脲组,每组8只。用无钙台式液灌流10 min,停灌30 min再灌注45 min模拟心肌缺血再灌注损伤模型。检测各组心肌细胞钙-镁-ATP(Ca2+-Mg2+-ATP)酶、钠-钾-ATP(Na+-K+-ATP)酶活性及全细胞膜片钳技术的电流电压钳模式记录各组心室肌细胞的ATP敏感钾通道(KATP通道)电流变化。结果在缺血的基础上,中药复方冠心康可使KATP通道进一步开放,通道电流明显增大,与KATP通道开放剂吡那地尔具有同等开放效应(P>0.05)。与模型组比较,冠心康组Ca2+-Mg2+-ATP酶、Na+-K+-ATP酶含量明显增高(P<0.05)。结论中药复方冠心康对于心肌缺血再灌注损伤具有一定的干预作用,促进KATP通道开放,减轻Ca2+内流,抑制Ca2+超载可能是冠心康在心肌缺血过程中发挥干预作用的有效途径。

英文摘要:

Objective To investigate the effect of Guanxinkang(GXK) on ATP-sensitive potassium channel in myocardial cells of rat with ischemic/reperfusion injury and its possible mechanism for cardiac vascular protection and anti-myocardial ischemia.Methods Wistar rats were established into I/R injured models by 10 min perfusion―30 min no-flow ischemia―45 min reperfusion,and divided into 5 groups: the I/R model group and 4 treatment groups treated respectively with glibenclamide,pinacidil,GXK and GXK+glibenclamide.Rats’ heart were isolated for detecting Ca2+-Mg2+-ATPase,Na+-K+-ATPase activity in myocardial cells,and the changes of current in ATP-sensive potassium channel(KATP) was recorded by whole patch clamp technique.Data were controlled by those taken from normal rats in a control group.Results KATP in the GXK treated group were higher than that in the I/R model group;and similar to that in the pinacidil treated group(P>0.05).As compared with the model group,activities of Ca2+-Mg2+-ATPase and Na+-K+-ATPase in the GXK treated group were increased significantly(P<0.05).Conclusion GXK shows definite intervention effect on myocardial I/R injury;which is possibly by way of furthering the opening of KATP channel,decreasing Ca2+ influx,and inhibiting Ca2+ overload.

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