细胞内钙在脑心综合征心律失常中作用研究

The study on the effects of intracellular calcium in arrhythmia resulted from cerebral-xardiac syndrome

目的通过研究脑心综合征心肌细胞内游离钙离子浓度([Ca2+]i)的变化及其来源,以探讨其与脑心综合征心律失常的关系。方法线栓法建立脑心综合征模型,监测心电图,酶法分离心肌细胞,激光共聚焦扫描显微镜观察心室肌[Ca2+]i的变化及其途径。结果模型组QT间期较正常组和假手术组明显延长(P<0.01);在正常台氏液中,KCl诱发模型组心肌[Ca2+]i升高幅度高于假手术组(P<0.01),用1μmol·L-1和10μmol·L-1维拉帕米预孵育模型组后,10μmol·L-1维拉帕米明显降低KCl诱发的心肌[Ca2+]i升高幅度(P<0.01);在无钙台氏液中,caffeine诱发模型组心肌[Ca2+]i升高幅度高于假手术组(P<0.01)。结论通过心肌细胞L-型钙通道和肌浆网雷诺定受体介导的内钙异常升高可能是脑心综合征心律失常的原因之一。

Aim To explore the relationship between calcium and arrhythmia resulted from cerebral-cardiac syndrome （CCS） by studying the change and its source of the myocardium Intracellular free calcium concentration. Methods The CCS model was produced by occluding right middle cerebral artery with nylon thread. The ECG were monitored. Cadiocyte were then isolated enzyme. The changes and pathway of the ventricular myoeytes [Ca^2＋]i were observed with Laser Scanning Confocal Microscope. Results QT intervals in CCS group were remarkably longer than that in sham group and normal group（P 〈0.01 ）. [Ca^2＋]i increasing induced by KCI in CCS group was significantly higher than that in sham group in Tyrode＇ s solution （P 〈 0. 05 ） ; [Ca^2＋]i increasing induced by KCl was obviously inhibited by 10 umol·L^-1 verapamil（ P 〈 0.01 ） after preincubation with verapamil （ 1 umol·L^-1 and 10umol·L^-1） in CCS group in tyrode＇s solution. [Ca^2＋]i increasing induced by caffeine in CCS group was significantly higher than that in sham group in calcium free tyrode＇s solution（ P 〈 0. 01 ）. Conclusion Abnormal [Ca^2＋]i increasing mediated by L-calcium channel and ryanodine receptor in sarcoplasmic reticu- lum may be one of the reasons of arrhythmia resulted from CCS.