论文部分内容阅读
实验用全细胞膜片箝技术 ,观察正常及缺血条件下 ,兔心内膜下心室肌细胞与心外膜下心室肌细胞的动作电位和稳态外向钾流及其变化。结果显示 :(1)正常条件下 ,心外膜下心室肌细胞与心内膜下心室肌细胞动作电位形态有差异 ,心外膜下心室肌细胞动作电位时程 (APD)较短 ,复极 1期后有明显的切迹 ,动作电位形态是“锋和圆顶” ,而心内膜下心室肌细胞APD较长 ,并且没有上述动作电位形态特征。这两类细胞静息电位无差异。 (2 )在缺血条件下 ,心外膜下的心室肌细胞动作电位复极 1期后切迹消失 ,且APD缩短程度明显大于心内膜下的心室肌细胞。 (3)在正常条件下 ,心外膜下心室肌细胞稳态外向钾流密度显著大于心内膜下心室肌细胞。 (4 )在缺血条件下 ,心外膜下心室肌细胞的稳态外向钾流的增加超过心内膜下的心室肌细胞 ,用优降糖可以部分逆转上述变化。实验结果提示 :增加的稳态外向钾流大部分是由于缺血造成细胞内ATP缺乏 ,致使IK ATP通道开放 ,钾外流
The whole-cell patch-clamp technique was used to observe the action potentials and steady-state outward potassium flux of subendocardial ventricular myocytes and subendocardial ventricular myocytes under normal and ischemic conditions in rabbits. The results showed that: (1) under normal conditions, the subependymal ventricular myocytes and subendocardial ventricular myocytes under different action potential morphology, subepithelial ventricular myoelectric action potential duration (APD) is shorter, repolarization After 1, there are obvious notch, action potential morphology is “front and dome”, and subendocardial ventricular myocytes APD longer, and there is no morphological characteristics of the above action potential. There was no difference in resting potential between these two types of cells. (2) Under the condition of ischemia, the notch of disappearance of the action potential of epicardial subventricular ventricular myocytes after repolarization for one period, and the shortening of APD was obviously greater than that of subendocardial ventricular myocytes. (3) Under normal conditions, steady-state outward potassium efflux density of subendocardial ventricular myocytes was significantly greater than that of subendocardial ventricular myocytes. (4) Under ischemic conditions, steady-state outward potassium flux in subependymal ventricular myocytes increased more than that in subendocardial ventricular myocytes, which were partially reversed by glyburide. The experimental results suggest that the increased steady-state outward potassium flux is largely due to an intracellular ATP deficiency caused by ischemia resulting in opening of the IK ATP channel, efflux of potassium