摘要
探讨Ｍｇ２＋对低氧心肌细胞保护作用的离子通道机制。方法采用膜片钳全细胞记录技术及细胞内透析的方法观察低氧时Ｍｇ２＋对心肌细胞钾电流、钙电流、Ｎａ＋－Ｃａ２＋交换电流及短暂性内向电流的调节作用。结果对１０个细胞观察显示常氧时细胞内１０ｍｍｏｌ／ＬＭｇ２＋对动作电位无明显影响，但可显著抑制低氧时动作电位时程的缩短（Ｐ＜０．０５），同时细胞内Ｍｇ２＋对１０分钟低氧引起的外向性钾电流有明显的抑制作用，对１０个细胞观察显示除极至０ｍＶ时其电流值从对照的２１３０±２４３ｐＡ降至１１８９±２１１ｐＡ，Ｐ＜０．０１；在常氧时细胞外１０ｍｍｏｌ／ＬＭｇ２＋对Ｎａ＋、Ｃａ２＋交换电流有部分抑制作用，细胞外Ｍｇ２＋可显著降低复氧早期短暂性内向电流的诱发率。结论细胞内Ｍｇ２＋可抑制低氧心肌细胞Ｋ＋外流，并对维持细胞内高钾及心肌细胞膜的正常兴奋性有重要意义。而细胞外Ｍｇ２＋对防止心肌缺血再灌流引起的钙超载有一定的作用。
Objective To determine effects of Mg 2+ on potassium current, transient inward current (lti) and Na + Ca 2+ exchange current in isolated ventricular myocytes during hypoxia. Methods Single myocytes were isolated from ventricles of adult guinea pig hearts. The patch clamp technique in whole cell configuration was used to study ionic currents, and experiments were performed in an experimental chamber that allows the cell to be exposed to a sufficiently low O 2 pressure. Results The 10 mmol/L intracellular free Mg 2+ (Mg 2+ i) had no effect on action potential abbreviation under normoxic condition, however, the action potential abbreviation during hypoxia was markedly inhibited in presence of 10 mmol/L Mg 2+ i. The amplitude of hypoxia induced time independent outward K + current was also greatly reduced when applied 10 mmol/L Mg 2+ in pipette solution. In early reoxygenation, Iti occurred in 73% of myocytes, 10 mmol/L extracellular Mg 2+ during hypoxia and reoxygenation lowered incidence of Iti, 10 mmol/L Mg 2+ could partly inhibit the Na + Ca 2+ exchange current in normoxic condition. Conclusion Intracellular Mg 2+ could block hypoxia induced outward current through ATP sensitive potassium channels. Mg 2+ i plays an important role in preventing depletion of cellular K + and regulates beat to beat cardiac activity. Extracellular Mg 2+ most probably decreases the signs of calcium overload in early reoxygenation by inhibiting Na + Ca 2+ exchange.
出处
《中华医学杂志》
CAS
CSCD
北大核心
1997年第7期505-508,共4页
National Medical Journal of China
基金
卫生部科学研究基金
