过刊浏览

一氧化氮增加常氧和缺氧豚鼠心室肌细胞持续性钠电流

马季骅, 王宪沛, 张培华

武汉科技大学医学院心脏电生理研究室,武汉,430080

摘要

运用全细胞膜片钳记录缺氧条件下豚鼠心室肌持续性钠电流(INa.P)的变化及施加药物对其的影响,以探讨INa.P的本质及缺氧增大INa.P的机制.结果显示:(1)在常氧条件下,一氧化氮(NO)前体L-精氨酸(L-Arg)和供体硝普钠(SNP)浓度依赖性地增大INa.P;(2)INa.P随缺氧时间延长而增大,缺氧15 min后施加NO合酶(NOS)抑制剂L-硝基精氨酸甲酯(L-NAME),不能使增大的INa.P明显回复[(1.344±0.320)vs(1.301±0.317)pA/pF,P＞0.05,n=5]。

关键词： Persistent sodium current; Nitric oxide; Hypoxia; Myocardium

Nitric oxide increases persistent sodium current of ventricular myocytes in guinea pig during normoxia and hypoxia

Ma Jihua, Wang Xianpei, Zhang Peihua

Cardio Electrophysiological research Laboratory, Medical college, Wuhan University of Science and Technoloyg. Wuhan 430080, China

Abstract

Whole cell patch-clamp technique was used to record the changes of persistent sodium current (INa.P) and the effect of administered agents in ventricular myocytes of guinea pig to investigate the essence of INa.P and mechanism of increased INa.P of ventricular myocytes during hypoxia. The results showed: (1) Pro-NO L-arginine(L-Arg) and donor sodium nitroprusside (SNP) increased INa.P in a concentration- dependent manner in normoxia. (2) INa.P increased gradually with the prolongation of hypoxia time. After 15 min of hypoxia, administration of N(G)-nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, could not significantly recover the increased INa.P [(1.344 ± 320) vs (1.301 ± 0.317) pA/pF, P>0.05, n=5].

Key words: ;;;

收稿日期：　　录用日期：

通讯作者：　　E-mail:

引用本文：

马季骅, 王宪沛, 张培华. 一氧化氮增加常氧和缺氧豚鼠心室肌细胞持续性钠电流[J]. 生理学报 2004; 56 (5): .

Ma Jihua, Wang Xianpei, Zhang Peihua. Nitric oxide increases persistent sodium current of ventricular myocytes in guinea pig during normoxia and hypoxia. Acta Physiol Sin 2004; 56 (5): (in Chinese with English abstract).