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机构地区:[1]广州市第一人民医院,510180 [2]中山大学附属第二医院 [3]广东省心血管病研究所
出 处:《中华心律失常学杂志》2009年第2期150-154,共5页Chinese Journal of Cardiac Arrhythmias
基 金:广州市科技攻关引导项目(200423-E0331)
摘 要:目的研究β2肾上腺素受体(β2受体)对心肌梗死后心肌细胞L型钙通道电流(‰)的调控作用。方法Wistar大鼠随机分为正常对照和心肌梗死组,制作心肌梗死模型。分离心肌细胞,应用全细胞膜片钳技术,观察心肌梗死后ICaL变化,先后给予β2受体激动剂salbutamol(10μmol/L)及β2受体阻滞剂ICI118,551(0.1μmol/L)后再观察ICaL的变化。结果心肌梗死后8周ICaL显著减低37.0%(P〈0.05)。在正常和梗死后8周后心肌细胞,β2受体激动剂均显著增加ICaL(P〈0.05),心肌梗死后对ICaL的调节作用较正常心肌细胞增强(23.4%±1.7%对33.1%±3.3%,P〈0.05),这种作用可被抑制型G调节蛋白(Gi蛋白)抑制剂放大,被环磷酸腺苷依赖蛋白激酶(PKA)拈抗剂抑制。结论β2受体对ICaL具有调节作用,且心肌梗死后这种调节作用增强,提示心肌梗死后β2受体在恶性心律失常发生中的作用可能提高。Objective To investigate the regulatory effects of β2-adrenergic receptor(β2-AR) on L- type calcium current (ICaL) in myocytes from infarcted heart. Methods Adult Wistar rats were randomly divided into two groups, the control group and the post-myocardial infarction ( MI ) group. The rat chest was opened and the left anterior descending coronary artery was ligated. The control group rats underwent sham-operated without coronary artery ligation. Myocytes were enzymatically disassociated by Langedorff perfusion. The whole cell-patch clamp recording technique was used to record ICaL in specific pipette solution and superfusion according to specific holding potential and command potential program. The responses of cardiomyocytes to IB2- AR agonist salbutamol ( 10 μmol/L)and then to β2-AR antagonist ICI118,551 (0. 1 μmol/L)were examined. Results ICaL in ventricular myocytes from the border zone of infarcted heart decreased by 37.0% significantly after MI( P 〈0. 05 ). β2-AR agonist increased ICaL more dramatically in myocytes from post-MI heart than in controls(23.4%±1.7% vs 33.1% ±3.3%, P〈0.05). Conclusion The regulatory effects of β2-AR on ICaL in myocytes are stronger after MI. It was suggested that β2-AR may responsible for the genesis of malignant arrhythmia after MI.
分 类 号:R542.22[医药卫生—心血管疾病]
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