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目的观察血管紧张素III(AT1)型受体阻断剂厄贝沙坦(irbesartan)预处理对大鼠心肌缺血再灌注性心律失常的保护作用,并探讨其可能机制。方法实验动物经厄贝沙坦预处理1周后,相对于对照组和手术组,应用体外心脏灌流方法在体外心脏上观察再灌注45min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45min内动作电位的变化;同时我们检测心肌标本AT1受体及肌浆网钙ATP酶(sar coplasmicreticulum Ca2+-ATPase,SERCA) mRNA表达水平的变化。结果厄贝沙坦组在再灌注45min内平均室速、室颤事件明显减少(P<0.01),且在再灌注45min内动作电位改善明显;同时发现,相对于对照组,手术组心脏AT1 mRNA表达升高而SERCA mRNA表达下调,厄贝沙坦可逆转上述表达变化。结论厄贝沙坦具有晚期药理性预适应的抗再灌注性心律失常作用,其机制可能与动作电位的改善、阻断AT1的表达、逆转SERCA mRNA水平下降,从而减少细胞内钙超载有关。
Objective To investigate the protective effect of irbesartan, an angiotensin III receptor blocker, on myocardial ischemia-reperfusion arrhythmias in rats and its possible mechanism. Methods The experimental animals were treated with irbesartan for 1 week. Compared with the control group and the surgery group, the in vitro cardiac perfusion method was used to observe the occurrence of ventricular arrhythmia and the suspension microelectrode method in the heart The changes of action potentials were observed within 45 minutes after reperfusion. At the same time, we detected the mRNA expression of AT1 receptor and sarcoplasmic reticulum Ca2 + -ATPase (SERCA) in myocardium. Results The mean VT and ventricular fibrillation events in irbesartan group decreased significantly (P <0.01) within 45 minutes after reperfusion, and the action potentials were significantly improved within 45 minutes after reperfusion. At the same time, compared with the control group, AT1 mRNA Increased expression of SERCA mRNA expression down, irbesartan can reverse the above expression changes. Conclusion Irbesartan possesses the late pharmacological preconditioning anti-reperfusion arrhythmia. Its mechanism may be related to the improvement of action potential, blocking the expression of AT1, reversing the decrease of SERCA mRNA level and decreasing the intracellular calcium overload.