首都医科大学学报 ›› 2006, Vol. 27 ›› Issue (6): 778-780.

• 基础研究 • 上一篇    下一篇

缺血再灌注小鼠心肌细胞Na+/Ca2+交换电流的改变

张知非1, 侯晓丽1, 崔茜1, 臧益民2, 王军1   

  1. 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
  • 收稿日期:2005-09-29 修回日期:1900-01-01 出版日期:2006-12-24 发布日期:2006-12-24
  • 通讯作者: 王军

Changes of Na+/Ca2+ Exchange Current in Ischemic Reperfused Cardiac Myocyte of Mouse

Zhang Zhifei1, Hou Xiaoli1, Cui Qian1, Zang Yimin2, Wang Jun1   

  1. 1. Department of Physiology, Capital University of Medical Sciences;2. Department of Physiology, The Fourth Military Medical University
  • Received:2005-09-29 Revised:1900-01-01 Online:2006-12-24 Published:2006-12-24

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8 min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+50 mV,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.

关键词: Na+/Ca2+交换电流, 缺血再灌注, 心室肌细胞, 膜片钳

Abstract: Objective To investigate the direct effects of ischemia/ reperfusion on Na+/Ca2+ exchange current in mouse cardiac myocyte and the mechanism of [Ca2+] overload induced by ischemia/reperfusion.Methods The electrogenic Na+/Ca2+ 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+/Ca2+ 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+/Ca2+ exchanger which maybe mainly responsible for the [Ca2+] overload during ischemia/reperfusion.

Key words: Na+/Ca2+ exchange current, ischemia/reperfusion, ventricular myocyte, patch clamp

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