摘要
目的：观察降钙素基因相关肽（ＣＧＲＰ）对家兔正常及缺血心肌电生理的影响，探讨其抗心律失常的电生理学机制．方法：在开胸兔急性心肌缺血模型上应用浮置微电极技术，记录心室肌细胞电位（ＴＭＰ）．结果：ＣＧＲＰ能够显著增加心室肌细胞静息电位，提高动作电位幅度（Ｐ＜０．０１）；心肌缺血后，ＣＧＲＰ除有上述作用外，尚能明显延长复极化至３０％和５０％（ＡＰＤ３０，ＡＰＤ５０）的时程，分别由（９１．３±１７．５）ｍｓ和（９４．５±１８．４）ｍｓ延长至（１０９．４±１４．１）ｍｓ和（１２０．２±１６．８）ｍｓ（Ｐ＜０．０５）．而缩短复极化至１００％（ＡＰＤ１００）的时程，由（２４１．３±１７．３）ｍｓ缩短至（１９４．４±１０．３）ｍｓ（Ｐ＜０．０１）．从而逆转了心肌缺血的ＡＰＤ异常变化．结论：①ＣＧＲＰ对心肌电活动具有调节作用；对缺血心肌的电生理具有稳定和保护作用；②ＣＧＲＰ的抗缺血性心律失常的作用机制可能与其逆转缺血后的复极相异常变化有关．
Objective: Actions of calcitonin gene related peptide (CGRP) on either normal or myocardial ischemic electrophysiology were observed in the present study, and its electrophysiologic mechanism of antiarrhythmia was probed into. Methods: In the acute myocardial ischemia model of an open chest rabbit. Transmembrane potential (TMP) was recorded using the technique of floating microelectrode. Results: It was found that CGRP could increase ventricular myocardial resting potential and elevate the level of action potential ( P <0.01). After myocardial ischemia, CGRP could obviously prolong the durations of repolarization to 30% and 50% (APD 30 , APD 50 ) as well from (91.3±17.5) ms and (94.5±18.4) ms to (109.4±14.1) ms and (120.2±16.8) ms respectively ( P <0.05), and shortened the duration of repolarization to 100% (APD 100 ) significantly [from (241.3±17.3) ms to (194.4±10.3) ms] ( P <0.01). The abnormal changes of APD were therefore reversed. Conclusion: (1) CGRP had regulatory effects on myocardial electrical activity, and played a stable and protective role in ischemic myocardial electrophysiology; (2) The mechanism of CGRP's anti ischemic arrhythmia was related to its reversal of abnormal changes of repolarization phase after myocardial ischemia.
出处
《第四军医大学学报》
1996年第5期342-346,共5页
Journal of the Fourth Military Medical University
关键词
降钙素
相关肽
心肌电生理
心肌缺血
calcitonin gene related peptide myocardial electrophysiology myocardial ischemia cardiac arrhythmia
