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探讨雌激素对心血管保护作用的机制，采用标准玻璃微电极技术及全细胞膜片钳技术观察17β-雌二醇（ES）对豚鼠心室乳头肌细胞动作电价的影响及其对分离的豚鼠心室肌细胞的L型钙通道电流的作用。结果：30μmol／LES灌流心肌30min可明显缩短动作电位时程；复极20％动作电位时程及复极50％动作电位时程分别由146±22ms，213±21ms缩短至87±6ms，107±11ms（P均＜0．01）。1，10，20，30μmol／LES是浓度依赖性抑制L型钙通道电流（P均＜0．01），抑制率分别为8％，18％，33％，43％。结论：ES是一种内源性的钙离子通道拮抗剂，这可能是其心血管保护作用的重要机制之一．
To investigate the mechanism of estrogen on cardiovascular protection, the standard glass microelectrode technique and whole-cell patch clamp technique were used to observe the effect of 17β-estradiol (ES) on the action price of guinea pig ventricular papillary muscle cells and its effect on isolated guinea pig ventricular muscle The role of L-type calcium channel current in cells. Results: 30μmol / LES perfusion myocardial 30min significantly shortened the action potential duration; repolarization 20% action potential duration and repolarization 50% action potential duration shortened from 146 ± 22ms, 213 ± 21ms to 87 ± 6ms, 107 ± 11ms ( P <0.01). 1, 10, 20 and 30μmol / LES inhibited the L-type calcium current in a concentration-dependent manner (P <0.01). The inhibitory rates were 8%, 18%, 33% and 43%, respectively. Conclusion: ES is an endogenous calcium channel antagonist, which may be one of its important mechanisms of cardiovascular protection.