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目的 :观察福辛普利预处理大鼠 2 4h后 ,对大鼠心肌缺血再灌注性心律失常的保护作用。方法 :实验动物于 2 4h前经福辛普利处理后 ,分别应用体外心脏灌流方法在体外心脏上观察再灌注 30min内室性心律失常的发生和悬浮微电极方法在体内心脏观察再灌注 30min内动作电位的变化。结果 :福辛普利组在再灌注 30min内室性心律失常的发生率和持续时间明显减少 (P <0 .0 1) ,心功能明显改善。提前应用缓激肽受体拮抗剂Hoe14 0、一氧化氮合酶抑制剂L NAME、ATP敏感性钾通道阻滞剂格列苯脲可全部或部分阻断福辛普利的抗心律失常作用 ;福辛普利组在再灌注 30min内动作电位改善明显。结论 :福辛普利具有晚期药理性预适应抗再灌注性心律失常的作用 ,其机制可能与动作电位的改善、缓激肽、一氧化氮和K+ ATP通道有关。
Objective: To observe the protective effects of fosinopril on rat myocardial ischemia-reperfusion arrhythmia after 24 h preconditioning. Methods: The experimental animals were treated with fosinopril 24 hours later, respectively. The in vitro cardioplegia was used to observe the occurrence of ventricular arrhythmia and the suspension microelectrode method within 30 minutes after reperfusion in vitro. Action potential changes. Results: The incidence and duration of ventricular arrhythmia in fosinopril group decreased significantly (P <0.01) within 30 minutes after reperfusion, and heart function improved significantly. Early application of bradykinin receptor antagonist Hoe14 0, nitric oxide synthase inhibitor L NAME, ATP-sensitive potassium channel blocker glibenclamide can block the anti-arrhythmic effect of fosinopril in whole or in part; Fosinopril group within 30min after reperfusion to improve the action potential. CONCLUSION: Fosinopril has the effect of late pharmacological preconditioning against reperfusion arrhythmia. Its mechanism may be related to the improvement of action potentials, bradykinin, nitric oxide and K + ATP channels.