Objective:To investigate the intervention effects of Panax Notoginseng Saponins(PNS) on ACh-CaCl,2, induced atrial fibrillation and proiosystole in rats. MethodsAnimal model of atrial fibrillation was established by acetylcholine (ACh)-calcium chloride (CaCl,2,) mixture for tail intravenous injection. After monitoring dynamic electrocardiogram for 24 hours, the rats with typical electrocardiogram of atrial fibrillation were screened out, and then randomly divided into the normal group, model group and PNS group. Each group was received the corresponding intervention. The dynamic electrocardiogram monitoring for 24 hours was applied in each group until the end of the experiment. The morphological changes of heart were observed by light microscope after hematoxylin and eosin (HE) and Masson’s thrichrome staining. The serum level of IL-17A was detected by enzyme linked immunosorbent assay (ELISA).  Results:①Compared with the normal group, the duration of atrial fibrillation in the model group was significantly increased(P,<,0.05). Compared with the model group,the duration of atrial fibrillation in the PNS group was significantly decreased(P,<,0.05). ②Compared with the normal group, the proiosystole incidence in the model group was significantly increased(P,<,0.05). Compared with the model group,the proiosystole incidence in the PNS group was significantly decreased(P,<,0.05). ③Compared with the normal group, a large number of inflammatory cells infiltration and local necrosis in the myocardium and many collagen fibers were observed in the model group. Compared with the model group,the myocardial cells in the PNS group arranged in order, only a small amount of inflammatory cell infiltration and collagen deposition were found around the vessels(P,<,0.05). ④Compared with the normal group, the serum level of IL-17A in the model group was significantly increased(P,<,0.05). Compared with the model group,the serum level of IL-17A in the PNS group was significantly decreased(P,<,0.05).  Conclusion:PNS can significantly inhibit the atrial fibrillation and proiosystole induced by ACh-CaCl,2, in rats,and relieve the myocardial fibrosis induced by atrial fibrillation. Its mechanism may relate to the inhibition of inflammatory reaction.