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起搏对离体大鼠心脏再灌注诱导的室性心律失常的保护作用。

Protective effect of pacing on reperfusion-induced ventricular arrhythmias in isolated rat hearts.

作者信息

Takeda S, Satoh T, Osada M, Komori S, Mochizuki S, Tamura K

机构信息

Second Department of Internal Medicine, Yamanashi Medical University, Japan.

出版信息

Can J Cardiol. 1995 Jul-Aug;11(7):573-9.

PMID:7656192
Abstract

OBJECTIVES

To determine whether pacing would have a protective effect similar to preconditioning on reperfusion-induced ventricular arrhythmias and whether this protective effect would be induced by pacing-induced myocardial ischemia.

DESIGN

Isolated rat hearts (n = 36) were perfused by the Langendorff technique and the working heart mode. Global ischemia was induced for 10 mins followed by reperfusion for 15 mins. The control group had no pacing, while in the other groups, the hearts were electrically paced three times at 300, 400 and 600 beats/min, respectively, for 5 mins with 1 min intervals between pacings.

MAIN RESULTS

The incidence of reperfusion-induced ventricular fibrillation in controls was 100%, whereas that in the 300, 400 and 600 beats/min groups was reduced to 67% (not significant), 50% (P < 0.03) and 30% (P < 0.01), respectively. The mean duration of reperfusion-induced ventricular fibrillation was also significantly reduced in the 300, 400 and 600 beats/min groups compared with the control group. Coronary flow during pacing in the 400 and 600 beats/min groups, but not the 300 beats/min group, was reduced significantly compared with controls. In the 300 beats/min group, oxygen tension of the coronary effluent during pacing was decreased significantly, and proton production and lactate release of coronary effluent during pacing were increased significantly compared with the control group.

CONCLUSIONS

Pacing exerted a protective effect similar to preconditioning against reperfusion-induced ventricular arrhythmias. Pacing-induced mild myocardial ischemia, in which coronary flow was maintained, may be involved in the mechanism of this protective effect.

摘要

目的

确定起搏是否会对再灌注诱导的室性心律失常产生类似于预处理的保护作用,以及这种保护作用是否由起搏诱导的心肌缺血所引发。

设计

采用Langendorff技术和工作心脏模式灌注36只离体大鼠心脏。诱导全心缺血10分钟,随后再灌注15分钟。对照组不行起搏,而其他组的心脏分别以300、400和600次/分钟的频率进行三次电起搏,每次5分钟,起搏间隔为1分钟。

主要结果

对照组中再灌注诱导的心室颤动发生率为100%,而在300、400和600次/分钟起搏组中分别降至67%(无显著差异)、50%(P<0.03)和30%(P<0.01)。与对照组相比,300、400和600次/分钟起搏组中再灌注诱导的心室颤动平均持续时间也显著缩短。与对照组相比,400和600次/分钟起搏组起搏期间的冠状动脉血流量显著减少,但300次/分钟起搏组未出现此情况。在300次/分钟起搏组中,起搏期间冠状动脉流出液的氧张力显著降低,与对照组相比,起搏期间冠状动脉流出液的质子产生和乳酸释放显著增加。

结论

起搏对再灌注诱导的室性心律失常发挥了类似于预处理的保护作用。起搏诱导的轻度心肌缺血(冠状动脉血流量得以维持)可能参与了这种保护作用机制。

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