兔心室肌细胞电生理异质性研究——缺血对动作电位和钾流的影响  

A study on the electrophysiological heterogeneity of rabbit ventricular myocytes——the effect of ischemia on action potentials and potassium currents

作　　者：祁小燕[1] 施渭彬[2] 汪海宏[2] 张志雄[1] 徐有秋[2] 

机构地区：[1]上海中医药大学生理教研室,上海200032 [2]上海第二医科大学生理教研室,上海200025

出　　处：《生理学报》2000年第5期360-364,共5页Acta Physiologica Sinica

基　　金：supported by the National Natural Science Foundation of China(No.39470269)

摘　　要：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 。WT5”BZ] With the whole cell variant patch clamp technique, action potentials (AP) and outward potassium currents of rabbit ventricular myocytes isolated from subendocardium and subepicardium were recorded and their changes were observed under normal and ischemia conditions. The results showed that (1) under normal condition, there were differences in the AP figures between ventricular subendocardial and subepicardial myocytes. Action potentials recorded from subepicardial myocytes had shorter action potential duration (APD) and a notch between phases 1 and 2, compared with those of subendocardial myocytes. The resting potential had no significant difference between these two populations of the action myocytes; (2) under ischemia condition, the notch of action potentials of subepicardial myocytes disappeared and the APD was shortened even more, compared with that of subendocardial myocytes; (3) under normal condition, the density of steady state outward potassium currents of subepicardial myocytes was significantly greater than that of subendocardial myocytes; (4) under ischemia condition, the increase of steady state outward potassium currents of subepicardial myocytes was greater than that of subendocardial myocytes. Glybenclamide could partly reverse the above changes. It is suggested that the increase of steady state outward potassium currents during ischemia is mainly due to the opening of I K ATP channels as a result of the deficiency of intracellular ATP caused by ischemia.

关 键 词：心室肌细胞 电生理异质性 动作电位 缺血 外向钾流 

分 类 号：Q463[生物学—生理学] Q424