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目的观察卡托普利对大鼠在体心肌缺血再灌注性心律失常的抑制作用,探讨其作用机制。方法雄性Wistar大鼠随机分为3组:假手术组、缺血再灌注组、卡托普利+缺血再灌注组,每组8只。建立大鼠在体缺血再灌注性心律失常模型,记录室性早搏、室速、室颤持续时间以及发生率的变化;分离单个大鼠心室肌细胞,利用全细胞膜片钳技术观察卡托普利对L-型钙电流的影响。结果与假手术组比较,缺血再灌注性心律失常组总的室性早搏个数明显增多,室速和室颤的持续时间及发生率也明显增加,预先给予卡托普利后,总的室性早搏个数减少,室速和室颤的持续时间及发生率明显降低(与缺血再灌注组相比P<0.05);在膜片钳记录实验中,与对照组相比,卡托普利组能够明显抑制L-型钙电流(P<0.05)。结论卡托普利对大鼠在体缺血再灌注性心律失常有明显的抑制作用,而且可能通过抑制L-型钙电流而发挥其作用。
Objective To observe the inhibitory effect of captopril on myocardial ischemia-reperfusion arrhythmia in rats and its mechanism. Methods Male Wistar rats were randomly divided into 3 groups: sham operation group, ischemia reperfusion group, captopril + ischemia reperfusion group, 8 rats in each group. Rat models of ischemia-reperfusion arrhythmia were established. The changes of ventricular premature beats, ventricular tachycardia, duration of ventricular fibrillation and the incidence of ventricular fibrillation were recorded. Single ventricular myocytes were isolated and whole-cell patch-clamp Lee on the L-type calcium current. Results Compared with the sham operation group, the total number of ventricular premature beats in ischemic-reperfusion arrhythmia group increased significantly, and the duration and incidence of ventricular tachycardia and ventricular fibrillation also increased significantly. After pretreatment with captopril, the total chamber The number of premature premature beats decreased, the duration and incidence of ventricular tachycardia and ventricular fibrillation decreased significantly (P <0.05 compared with ischemia-reperfusion group). In the patch-clamp recording experiment, compared with the control group, Group can significantly inhibit L-type calcium current (P <0.05). Conclusions Captopril can obviously inhibit the ischemia-reperfusion arrhythmia in rats and may play its role by inhibiting L-type calcium current.