摘要
目的 :探讨缺血再灌注心律失常机制及地尔硫、汉防己甲素对其的干预作用。方法 :采用玻璃微电极技术以豚鼠乳头肌为研究对象观察模拟缺血再灌注过程中动作电位的变化及地尔硫、汉防己甲素对其的影响。结果 :对照组动作电位时程 (APD50、APD90)、有效不应期 (ERP)、动作电位振幅 (APA)随缺血时间延长而降低 ,含氧台氏液复灌20min恢复。5μmol/L地尔硫和10μmol/L汉防己甲素可缩短APD90、ERP ,对APA无影响。缺血过程中不能减少ERP、APD的缩短程度 ,但相对延长ERP ,减少再灌注心律失常发生。结论 :触发或自律性异常是再灌注心律失常的发生机制 ,钙离子超负荷发挥作用。地尔硫和汉防己甲素可减少再灌注心律失常的发生 ,但有潜在致折返性心律失常危险。
Objective:To investigate the mechanism of reperfusion arrhythmia and the antiarrhythmic effect of diltiaze and tetrandtine.Methods:Using microelectrode technique to record action potentials in ventricular papillary muscle.Results:APD and ERP shortened and APA deceased during ischemia while all the parameters recovered during reperfusion.APD and ERP were shortened by5μmol/L of diltiazem and10μmol/L of teˉtrandrine.The shortening effect of APD and ERP was not attenuated during reperfusion,ERP/APD90inˉcreased,and reperfusion arrhythmia abolished.Conclusion:Trigger activity or increased automaticity is one of mechanisms of reperfusion arrhythmia,and calcium overload plays an important role.Diltiazem and tetrandrine inhibit reperfusion arrhythmia,but have latent proarrhythmic effect.
出处
《天津医药》
CAS
北大核心
2003年第4期238-240,共3页
Tianjin Medical Journal
