脑心综合征大鼠心肌细胞内[Ca^(2+)]_i对KCl除极的反应性增强

The responsivity of [Ca^(2+)]_i of myocardial cells to KCl depolarization enhanced in rats with cerebro-cardiac syndrome

目的研究脑心综合征(cerebro-cardiac syndrome,CCS)心肌细胞内游离钙离子浓度([Ca2+]i)对KCl除极的反应性,通过心肌[Ca2+]i的变化来探讨脑心综合征心律失常的发生机制。方法用线栓法栓塞右侧大脑中动脉建立脑心综合征模型。采用酶法分离心肌细胞,Fluo-3/AM负载后采用激光共聚焦扫描显微镜观察心肌[Ca2+]i对KCl除极后的反应性。结果假手术组与正常组心室肌[Ca2+]i对KCl除极后的反应性无显著差别(P>0.05);模型组心室肌[Ca2+]i的升高幅度、速度以及不同时间点的恢复程度均显著高于假手术组(P<0.05);且加KCl后CCS24 h组心肌[Ca2+]i的上升速度明显高于CCS 2 h组(P<0.05),在扫描不同时间点恢复程度显著快于CCS 2 h组(P<0.05)。结论脑心综合征心肌[Ca2+]i在KCl除极后升高速度、幅度及恢复程度都发生改变,可能是脑心综合征心律失常发生机制之一。

Objective To investigate the mechanism of arrhythmia in cerebro-cardiac syndrome （CCS）in rats through the responsivity of [Ca^2＋]i to KCl depolarization in myocardial cells.Methods Twenty Wistar rats were randomly divided into normal group, sham group, CCS 2 h group find CCS 24 h group. The rat model of CCS was produced by occluding right middle cerebral artery. Myocardial cells were then isolated with Langendorff perfusion technique and [Ca^2＋]i was measured with calcium indicator Fluo-3/AM and laser scanning confocal microscope after giving KCl.Results There was no statistic difference in responsivity of cytosolic [Ca^2＋]i to KCl depola-rization between the sham group and the normal group （P〉0.05） ; The ascendant velocity, the extent of cytosolic [Ca^2＋]i elevation and the restoration in CCS 2 h group and 24 h group were significantly increased compared with sham group（P〈 0.05）;The ascendant velocity and the extent of restoration of cytosolic [Ca^2＋]i in CCS 24 h were quicker significantly than that in CCS 2 h group. Conclusion The ascendant velocity, the extent of cytosolic [Ca^2＋]i elevation and restoration in CCS increased significantly compared with normal group after KCl depolarization and that may be one of the mechanisms of arrhythmia in cerebro-cardiac syndrome,.