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目的:研究再灌注心律失常发生机制及维拉帕米的保护作用.方法:采用标准微电极细胞电生理方法.结果:对照组RMP,APA,APD50,Vmax,ERP随缺血时间的延长而降低,随正常充氧台氏液的复灌而回复,20分钟后恢复对照状态.维拉帕米治疗组复灌20分钟除ERP,APD90外APA,APD50,Vmax未恢复至对照状态.对照组10例标本均发生了再灌注心律失常,6/10例为室早,5/6例于复灌4.5±2.6分钟时出现DAD或EAD,并发生触发性室早.4/10例发生持续性心动过速,持续10.4±5.0分钟.快速起搏可以超速抑制,但不能终止.治疗注组8/10例未出现心律失常,仅2/10例发生室早,均未记录到EAD或DAD.结论:触发活动及自律性增高是再灌注心律失常的主要发生机制,维拉帕米可有效地拮抗再灌注心律失常的发生.
Objective: To study the mechanism of reperfusion arrhythmia and the protective effect of verapamil.Methods: Standard microelectrode cell electrophysiological method was used.Results: The RMP, APA, APD50, Vmax, ERP in the control group decreased with the prolongation of ischemia , Returned to control with the reperfusion of normal oxygenated Tyrodes solution, and returned to the control state after 20 minutes.After 20 minutes of reperfusion in the verapamil group, APA, APD50 and Vmax did not recover to the control except ERP Recurrence arrhythmias occurred in 6 of 10 cases, DAD or EAD occurred in 5 of 6 patients with 4.5 ± 2.6 minutes of reperfusion, and triggered early ventricular arrest. In 4/10 patients with persistent heartbeat Fasting continued for 10.4 ± 5.0 minutes. Rapid pacing could be over-suppressed but not terminated. No EAD or DAD was recorded in 8/10 patients without arrhythmia and only 2/10 premature ventricular contractions. : Triggered activity and increased self-discipline is the main mechanism of reperfusion arrhythmia, verapamil can effectively antagonize the reperfusion arrhythmia.