摘要
目的 探讨苯肾上腺素诱导兔心室肌细胞肥大过程中心肌细胞电生理特性的改变及意义.方法将24只新西兰乳兔随机分为苯肾上腺素组和正常对照组各12只.体外原代培养乳兔心室肌细胞,苯肾上腺素组给予10 μmol/L苯肾上腺素持续作用48 h后,应用全细胞膜片钳技术观察心室肌细胞膜电容、动作电位时程和快激活延迟整流钾电流的变化,并与对照组比较.结果 苯肾上腺素作用48 h后,心室肌细胞膜电容较正常对照组增加36.4%（P＜0.01）;心室肌细胞动作电位复极达90%时限较对照组延长18.8%（P＜0.01）;心室肌细胞快激活延迟整流钾电流尾电流密度较对照组下调24.1%（P＜0.05）.结论 苯肾上腺素长期持续刺激可诱导心室肌细胞肥大并发生电重构,可能是导致室性心律失常发生的一个重要机制.
Objective To explore the changes and the significance of electrophysiological characteristics of the cultured hypertrophic neonatal rabbit ventricular myocytes induced by phenylephrine. Methods Twentyfour New Zealand neonatal rabbit were randomly divided into phenylephrine group （n=12） and normal control group （n= 12 ）. Ventricular myocytes isolated from phenylephrine group were cultured under stimulation of phenylephrine for 48 hours. Myocyte membrane capacitance, action potential duration and rapidly activated delayed rectifier potassium current were measured by the whole cell Patch-clamp technique 48 hours after phenylephrine stimulation. Results Compared with those of control group, 48 hours after phenylephrine stimulation, ventricular myocyte capacitance increased by 36.4%（P〈0.01 ）, action potential duration at 90% repolarization of ventricular myocytes was prolonged by 18.8%（P〈0.01 ）, tail current density of rapidly activated delayed rectifier potassium current of ventrieular myocytes decreased by 24.1%（P〈0.05）. Conclusion Long-standing phenylephrine stimulation could produce the electrophysiological remodeling of hypertrophied ventricular myoeytes, which could be an important mechanism of ventricular arrhythmia.
出处
《中国心血管病研究》
CAS
2011年第6期440-443,共4页
Chinese Journal of Cardiovascular Research
关键词
心肌
肥大
苯肾上腺素
电生理
兔
室性心律失常
Myocardium
Hypertrophy
Phenylephrine
Electrophysiology
Rabbits
Ventricular arrhythmia
