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目的研究槐果碱的抗心律失常作用及其机制。方法采用乌头碱诱发的快速型心律失常的SD大鼠,分为模型组、槐果碱组(5 mg·kg~(-1),iv)与胺碘酮组(2.5μg·kg~(-1),iv)3组。心电图连续示波观察,电脑实时显示并存储,记录室性早搏、室性心动过速、心室扑动-心室颤动、心脏停搏出现时间,换算成乌头碱的累积量(μg·kg~(-1)),研究其抗心律失常的作用。运用玻璃微电极记录豚鼠心室乳头肌动作电位,研究槐果碱(1、5、10μmol·L~(-1))对心室乳头肌动作电位时程(APD)、有效不应期(ERP)、最大除极化速度(V_(max))、动作电位幅度(APA)、静息电位(RP)的影响。结果槐果碱组和胺碘酮组与模型组相比均能推迟室性早搏、室性心动过速、心室扑动-心室颤动、心脏停搏的出现时间,两者均能增加引起上述心律失常时乌头碱的耗量(P<0.05),但在槐果碱与胺碘酮两者间无差异(P>0.05)。槐果碱(1、5、10μmol·L~(-1))均能使APD_(50)、APD_(90)、APD_(100)、ERP延长,V_(mas)减小(P<0.05),但对APA、RP的影响无显著差异(P>O.05)。结论槐果碱能抑制乌头碱诱发的快速型心律失常,与其延长APD和ERP有关。
Objective To study the antiarrhythmic effect of sophocarpine and its mechanism. Methods Acute arrhythmia induced by aconitine in SD rats was divided into model group, sophocarpine group (5 mg · kg -1, iv) and amiodarone group (2.5 μg · kg ~ (-1) -1), iv) 3 groups. Electrocardiogram continuous oscillographic observation, the computer real-time display and storage, recording ventricular premature beats, ventricular tachycardia, ventricular fibrillation - ventricular fibrillation, cardiac arrest time, converted to the accumulation of aconitine (μg · kg ~ ( -1)) to study its anti-arrhythmic effect. The action potentials of guinea pig ventricular papillary muscles were recorded by glass microelectrode to study the effects of sophocarpine (AP), effective refractory period (ERP) Maximum depolarization speed (V_ (max)), action potential amplitude (APA), resting potential (RP) effects. Results Both the sophocarpine group and the amiodarone group were able to delay premature ventricular contractions, ventricular tachycardia, ventricular fibrillation-ventricular fibrillation and cardiac arrest when compared with the model group, both of which could increase the above-mentioned cardiac rhythm Abnormal aconitine consumption (P <0.05), but in the sophocarpine and amiodarone no difference between the two (P> 0.05). (1, 5, 10μmol·L -1) could prolong APD_ (50), APD_ (90), APD_ (100), ERP and decrease V mas (P < However, there was no significant difference between APA and RP (P> 0.05). Conclusion Sophocarpine can inhibit aconitine-induced tachyarrhythmia, which is related to the prolongation of APD and ERP.