心肌梗死后β2受体对心肌细胞L型钙通道电流的调控作用

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。

The regulation effects of β2-adrenergic receptor on ICaL in myocytes from infarcted heart

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 di-vided 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-op-erated 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 β2-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 respen sible for the genesis of malig-nant arrhythmia after MI.