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目的:探讨参松养心胶囊降低心房颤动(房颤)的发生的具体机制。方法:杂种犬18只,随机分为对照组(n=6)、起搏组(n=6)和参松组(n=6)。对照组植入起搏器后程控关闭起搏器;起搏组植入起搏器后长期间断起搏右房(400次/min,8h/d);参松组植入起搏器后长期间断起搏并每天喂养参松养心,所有犬喂养8周。12周后进行心房电生理和生化指标检测。结果:与对照组相比,起搏组和参松组犬的心房有效不应期(AERP)明显降低,且房颤的诱发次数和持续时间均明显升高;但参松组犬的AERP和房颤诱发明显低于起搏组犬。8周后,起搏组和参松组犬血清和心房肌炎性因子水平和心房交感神经密度明显高于对照组,而乙酰胆碱水平和α7烟碱型乙酰胆碱受体(a7nAChR)蛋白表达低于对照组;但参松组犬的血清和心房肌炎性因子水平和心房交感神经密度明显低于起搏组,而乙酰胆碱水平和a7nAChR蛋白表达高于起搏组。结论:参松养心抑制心房肌电重构和阵发性房颤的诱发可能与其调节胆碱能抗炎通路有关。
Objective: To explore the specific mechanism of Shensong Yangxin Capsule to reduce the occurrence of atrial fibrillation (AF). Methods: 18 hybrid dogs were randomly divided into control group (n = 6), pacing group (n = 6) and shensong group (n = 6). The control group was programmed to turn off the pacemaker after the pacemaker was implanted. The pacing group was pacing the right atrium for a long time after implantation of the pacemaker (400 / min, 8h / d) Intermittent pacing and daily feeding Senate heart, all dogs were fed for 8 weeks. Atrial electrophysiological and biochemical tests were performed 12 weeks later. Results: Compared with the control group, the atrial effective refractory period (AERP) and the duration of atrial fibrillation were significantly increased in the pacing group and the control group. However, the AERP and Atrial fibrillation evoked significantly lower than pacing dogs. After 8 weeks, serum and atrial myositis inflammatory factor levels and atrial sympathetic nerve density in pacing group and ginseng group were significantly higher than those in control group, while the levels of acetylcholine and α7 nicotinic acetylcholine receptor (a7nAChR) Group. However, the serum and atrial myocyte inflammatory factor levels and atrial sympathetic nerve density in the canine group were significantly lower than those in the pacing group, while the levels of acetylcholine and a7nAChR protein were higher than those in the pacing group. Conclusion: Shensongyangxin inhibits atrial electrical remodeling and induction of paroxysmal atrial fibrillation may be related to its regulation of cholinergic anti-inflammatory pathways.