缺血再灌注小鼠心肌细胞Na^+/Ca^(2+)交换电流的改变  

Changes of Na^+/Ca^(2+) Exchange Current in Ischemic Reperfused Cardiac Myocyte of Mouse

作　　者：张知非[1] 侯晓丽[1] 崔茜[1] 臧益民[2] 王军[1] 

机构地区：[1]首都医科大学生理学教研室 [2]第四军医大学生理学教研室

出　　处：《首都医科大学学报》2006年第6期778-780,共3页Journal of Capital Medical University

基　　金：北京市优秀人才基金;国家教育部留学回国启动基金(20042D0501815)资助项目

摘　　要：目的观察缺血再灌注损伤对小鼠心肌细胞Na+/Ca2+交换蛋白电流的直接影响,探讨缺血再灌注损伤中Ca2+超载的机制。方法采用全细胞打孔膜片钳技术,观察缺血再灌注损伤对急性分离的小鼠心室肌细胞Na+/Ca2+交换蛋白电流(INa/Ca)的影响。细胞外灌流代谢抑制剂(5 mmol/L氰化钠和10 mmol/L脱氧葡萄糖)模拟化学性心肌细胞缺血状态。结果缺血8m in明显抑制了小鼠心室肌细胞钠钙交换蛋白内向和外向电流〔在-100 mV,电流从(-0.04±0.01)nA减小到0 nA;在+50mV,电流从(0.25±0.08)nA减小到(0.11±0.03)nA〕。而随后的再灌注则导致钠钙交换蛋白电流迅速而明显的增大,尤以外向电流增大更加显著〔在+50 mV,电流从(0.25±0.08)nA增大到(0.49±0.12)nA〕。结论缺血再灌注直接影响小鼠心室肌细胞Na+/Ca2+交换蛋白的功能及状态,使Na+/Ca2+交换蛋白的反向转运功能明显增强,这种改变可能是导致缺血再灌注损伤中Ca2+超载的关键因素。Objective To investigate the direct effects of ischemia/reperfusion on Na^＋/Ca^2＋ exchange current in mouse cardiac myocyte and the mechanism of [ Ca^2＋ ] overload induced by ischemia/reperfusion. Methods The electrogenic Na^＋/Ca^2＋ exchanger currents was recorded from freshly isolated mouse ventricular myocyte during ischemia/reperfusion using nystatin-perforated patch clamp techniques. Myocardial ischemia was simulated by perfusion of metabolic inhibitor （5 mmol/L NaCN and 10 mmol/L deoxyglucose in glucose-free solution） and reperfusion was achieved by washing out the metabolic inhibitor. Results Ischemia significantly inhibited inward and outward Na^＋/Ca^2＋ exchanger currents [ from （ - 0.04 ± 0.01 ） nA to 0 nA at - 100 mV ; from （0.25 ±0.08 ） nA to （0.11 ± 0.03）nA at ＋50 mV], Subsequent reperfusion enhanced NCX current obviously, especially the outward currents [from （0.25 ±0.08） nA to （0.49 ± 0. 12 ）nA at ＋ 50 mV）. Conclusion The results suggest that ischemia/reperfusion result in significantly functional changes of Na ^＋/Ca^2＋ exchanger which maybe mainly responsible for the [ Ca^2＋ ] overload during ischemia/reperfusion.

关 键 词：Na^+/Ca^2+交换电流 缺血再灌注 心室肌细胞 膜片钳 

分 类 号：R322.11[医药卫生—人体解剖和组织胚胎学]