Chen You-Ren, Yi Fang-Fang, Li Xin-Yi, Wang Cheng-Yao, Chen Li, Yang Xin-Chun, Su Pi-Xiong, Cai Jun
Department of Cardiology, The Second Affiliated Hospital to Medical College, Shantou University, Shantou 515041, People's Republic of China.
Cardiovasc Drugs Ther. 2008 Dec;22(6):479-85. doi: 10.1007/s10557-008-6141-8. Epub 2008 Oct 14.
The effects of resveratrol treatment on ventricular arrhythmia, survival, and late cardiac remodeling were evaluated in rats with myocardial infarction (MI).
Three groups of rats (S: ham-operated, MI, and MI pre-treated with resveratrol) were treated in an in vivo MI model by ligation of left anterior descending coronary artery. The electrocardiogram signals were monitored and recorded for 24 h using an implanted telemetry transmitter. The incidence of ventricular arrhythmias during the first 24-h after MI was also evaluated. Meanwhile, invasive in vivo electrophysiology with pacing in the right ventricle was performed in each group to assess the inducibility of ventricular arrhythmias.
Administration of resveratrol significantly suppressed the MI-induced ventricular tachycardia and ventricular fibrillation (0.4 +/- 0.2 in Resv group vs. 7.1 +/- 2.2 in MI group episodes per hour per rat, P < 0.01). Data also showed that the incidence of inducible ventricular tachycardia was lower in the Resv group than the MI group (46% vs. 81%, P < 0.01). The infarct size and mortality in the Resv group at 14 weeks were reduced by 20% and 33%, respectively, compared with the MI groups. Results from patch clamp recording revealed that resveratrol inhibited L-type calcium current (I (Ca-L)), and selectively enhanced ATP-sensitive K(+) current (I (K,ATP)) in a concentration-dependent manner.
These results suggested that the emerging anti-arrhythmic character induced by resveratrol treatment in rat hearts could be mainly accounted for by inhibition of I (Ca-L) and enhancement of I (K,ATP). Administration of resveratrol also improved the long-term survival by suppressing left ventricular remodeling.
在心肌梗死（MI）大鼠中评估白藜芦醇治疗对室性心律失常、生存率和晚期心脏重塑的影响。
三组大鼠（假手术组、MI组和白藜芦醇预处理的MI组）在体内MI模型中通过结扎左冠状动脉前降支进行处理。使用植入式遥测发射器监测并记录心电图信号24小时。还评估了MI后最初24小时内室性心律失常的发生率。同时，对每组进行右心室起搏的有创体内电生理学检查，以评估室性心律失常的诱发性。
白藜芦醇给药显著抑制了MI诱导的室性心动过速和心室颤动（白藜芦醇组每只大鼠每小时发作0.4±0.2次，MI组为7.1±2.2次，P<0.01）。数据还显示，白藜芦醇组可诱导的室性心动过速发生率低于MI组（46%对81%，P<0.01）。与MI组相比，白藜芦醇组14周时的梗死面积和死亡率分别降低了20%和33%。膜片钳记录结果显示，白藜芦醇以浓度依赖性方式抑制L型钙电流（I(Ca-L)），并选择性增强ATP敏感性钾电流（I(K,ATP)）。
这些结果表明，白藜芦醇治疗在大鼠心脏中诱导的新出现的抗心律失常特性可能主要是由于抑制I(Ca-L)和增强I(K,ATP)。白藜芦醇给药还通过抑制左心室重塑提高了长期生存率。
