双心室起搏-不应期电刺激的急性血液动力学变化和离子机制

Acute homodynamic effects of biventricular pacing in SSS patients and its ionic mechanism

目的观察双心室起搏(BivP)对病态窦房结综合征(SSS)患者的急性血液动力学变化和心脏绝对不应期电刺激(ARPES)对豚鼠衰竭心室肌细胞钙离子流的影响。方法对10例SSS患者经冠状静脉左室后外侧支和右心室心尖部进行BivP,观察起搏前后5 min的心脏每分输出量(CO)、心脏排血指数(CI)、肺毛细血管嵌压(PCWP)和心电图QRS离散度(QRSd)、QT离散度(QTd)、跨室壁复数离散度(TDR)的变化。应用单细胞收缩动缘检测仪和膜片钳技术,观察ARPES前后单个豚鼠衰竭心室肌细胞收缩幅度、ICa-L、Ca-T的变化。结果BivP时CO、CI分别增加16.2%、16.8%,PCWP下降,TDR变小,表明BivP可增加心肌收缩功能,减小跨室壁复极离散度。ARPES使单个衰竭心室肌细胞收缩幅值和Ca-T分别增高15.5%和16.8%。结论ARPES可触发ICa-L开放,增加Ca-T,增强豚鼠衰竭心室肌细胞的收缩功能。BivP时一个电信号必然进入另一个电信号的绝对不应期,因此BivP-ARPES时ICa-L开放,Ca-T增加等,可能也是其改善心脏收缩功能的机制之一。

Objective To evaluate the acute homodynamic effects of biventricular pacing （BivP） in sick sinus syndrome （SSS） patients and investigate the Ca^2＋ changes during absolute refractory period electrical stimulation （ARPES） in failing guinea-pig ventricular myocyte. Methods The CO, CI, PCWP and ECG parameters were measured in ten patients with SSS before and after 5 min BivP connecting RVA＋ LVB. The extent of contraction and Ca^2＋ transient （Ca-T） changes of failure guinea-pig ventricular myocyte were recorded with the motion edge detection system. Results CO and CI increased by 16.2% and 16.8%, respectively. PCWP and TDR decreased during BivP, which suggested that BivP could improve systolic function and TDR. The contraction extent and Ca-T （F360/F380） of failure guinea-pig ventricular myocyte increased by 15.5 % and 16.8 %, respectively, during ARPES. It suggested that increased contractility of failure myocyte might be due to ICa-L and Ca^2＋ released from SR after appropriate ARPES. Conclusion Appropriate ARPES might strengthen contractility through increasing ICa-L and Ca-T of failing guinea-pig ventricular myocyte. One signal has conducted into another＇s ARP in BivP, so the changed ICa-L and Ca-T during BivP-ARPES may be one of the mechanisms of improving systolic function.