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目的探讨肾去交感神经(RSD)对长期右室起搏犬室性心律失常诱发的影响及机制。方法 21只比格犬随机分为对照组(n=7),心力衰竭(简称心衰)组(n=7)和RSD组(n=7)。对照组植入起搏器不起搏;心衰组植入起搏器后以240次/分的频率连续右室起搏3周;RSD组先行双侧肾动脉消融,后起搏器植入起搏右室3周。所有犬在起搏器植入前及3周后均进行心脏超声监测左右心室舒张末期内径,3周后开胸行心室电生理监测心室不应期、心室肌传导时间及室性心律失常的诱发,Masson染色和免疫组化法分别检测心室肌纤维化和Cx43表达。结果 2只犬实验中死亡,共19只犬完成实验。心衰组的心室肌QT间期和有效不应期比RSD组和对照组明显延长,心衰组的心室间传导时间明显长于RSD组和对照组[(77±9)ms vs(65±8)ms,(61±7)ms;P=0.03]。心室颤动诱发率在心衰组明显高于RSD组(19%vs 6.9%;P<0.05)。心衰组心室肌纤维化及CX43的异质性表达明显高于对照组和RSD组。结论 RSD可抑制长期右室起搏犬恶性室性心律失常的诱发,此可能与其抑制心室肌基质重构和电重构有关。
Objective To investigate the effects and mechanisms of renal denervation (RSD) on the induction of ventricular arrhythmia in long-term right ventricular pacing. Methods Twenty-one beagle dogs were randomly divided into control group (n = 7), heart failure group (n = 7) and RSD group (n = 7). Control group implanted pacemakers pacing; heart failure group implanted pacemakers to 240 beats / min frequency of continuous right ventricular pacing for 3 weeks; RSD group before bilateral renal artery ablation, after implantation of pacemaker Right ventricular pacing for 3 weeks. All dogs underwent echocardiographic monitoring of left and right ventricular end-diastolic diameter before and 3 weeks after implantation of the pacemaker. Three weeks later, they were subjected to ventricular electrophysiological monitoring of ventricular refractory period, ventricular conduction time and ventricular arrhythmias induced by Masson Staining and immunohistochemistry were used to detect ventricular fibrosis and Cx43 expression. Results Two dogs died in the experiment, a total of 19 dogs completed the experiment. The ventricular QT interval and effective refractory period in heart failure group were significantly longer than those in RSD group and control group. The ventricular conduction time in heart failure group was significantly longer than that in RSD group and control group [(77 ± 9) ms vs (65 ± 8) ) ms, (61 ± 7) ms; P = 0.03]. The incidence of ventricular fibrillation in HF group was significantly higher than that in RSD group (19% vs 6.9%; P <0.05). Heart failure group ventricular fibrosis and CX43 heterozygous expression was significantly higher than the control group and the RSD group. Conclusion RSD can inhibit the induction of malignant ventricular arrhythmia in long-term right ventricular pacing, which may be related to its inhibition of ventricular remodeling and electrical remodeling.