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研究缺血预适应 (IPC)抗心律失常的机制。采用玻璃微电极技术 ,观察 IPC对模拟缺血 复氧灌流过程中大鼠乳头肌动作电位 (AP)、有效不应期 (ERP)的影响。结果 :IPC过程中 AP进行性缩短。IPC使其后缺血 1～ 5 min时静息膜电位 (RMP)、AP幅度 (APA)、复极 90 %的 AP时程 (APD90 )、ERP、零相最大上升速度 (Vmax)迅速缩短或降低 ,IPC促进了缺血 3 0 min时上述参数的明显改善 ;IPC限制了复氧灌流时 APD90 的过度延长 ,并使 RMP超极化。ATP敏感性钾通道的加速开放与上述改变有关。结论 :IPC加速 ATP敏感性钾通道的开放 ,迅速缩短 APD和 ERP,降低膜电位 ,导致心肌细胞兴奋性降低及丧失 ,此可能是其抗缺血早期心律失常的机制之一。通过改善缺血晚期不应期离散度及缓慢传导的程度 ,减少 相折返 ,则是其抗缺血晚期心律失常的可能机制。IPC限制了复氧灌流时 APD90 的过度延长 ,从而减少内向离子流及触发活性 ,此可能与其抗再灌流心律失常有关。
To study the mechanism of ischemic preconditioning (IPC) against arrhythmias. The glass microelectrode technique was used to observe the effect of IPC on the AP and effective refractory period (ERP) of the rat papillary muscles during simulated ischemia reperfusion. Results: AP was progressively shortened during IPC. IPC reduced the resting membrane potential (RMP), AP amplitude (APA), APD90 with 90% repolarization, ERP, Vmax rapidly shortened from 1 to 5 min after ischemia or IPC promoted the significant improvement of the above parameters at 30 min of ischemia; IPC restricted the excessive prolongation of APD90 during reperfusion and hyperpolarized RMP. The acceleration and opening of ATP-sensitive potassium channels are related to the above changes. CONCLUSION: IPC accelerates the opening of ATP-sensitive potassium channels, rapidly shortening APD and ERP, decreasing membrane potential and decreasing and excitability of cardiomyocytes, which may be one of the mechanisms of anti-ischemic early arrhythmia. By improving the degree of delayed refractory refractory period and the degree of slow conduction and reduce phase reentry, it is its possible mechanism of anti-ischemic late arrhythmia. IPC limits the excessive prolongation of APD90 during reoxygenation, thus reducing the inward ion flux and triggering activity, which may be related to its anti-reperfusion arrhythmia.