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目的:探讨血管紧张素Ⅱ诱导心肌肥大过程中心肌细胞电生理特征性改变及意义。方法:将24只新西兰兔随机分为血管紧张素Ⅱ组和正常对照组各12只,体外培养乳兔心室肌细胞,观察10-7mol/L血管紧张素Ⅱ作用48 h心肌细胞动作电位时程、瞬时外向钾电流密度的变化,并与对照组比较。结果:血管紧张素Ⅱ组心室肌细胞膜电容较正常对照组增加38.22%(P<0.01);心室肌细胞动作电位复极达90%时限较对照组延长22.1%(P<0.01);心室肌细胞瞬时外向钾电流密度较对照组下调28.6%(P<0.05)。结论:血管紧张素Ⅱ持续刺激可引起心室肌细胞电重构,可能是导致室性心律失常发生的一个重要机制。
Objective: To investigate the changes of electrophysiological characteristics of cardiomyocytes induced by angiotensin Ⅱ in cardiac hypertrophy and its significance. Methods: Twenty-four New Zealand white rabbits were randomly divided into angiotensin Ⅱ group and normal control group, 12 rabbits were cultured in vitro. The effects of 10 -7 mol / L Angiotensin Ⅱ on cardiomyocyte action potential duration , Transient outward potassium current density changes, and compared with the control group. Results: The membrane capacitance of ventricular myocytes increased by 38.22% (P <0.01) in angiotensin Ⅱ group compared with that of control group (P <0.01). The duration of 90% repolarization of ventricular myocytes increased by 22.1% (P <0.01) The transient outward potassium current density was 28.6% lower than that of the control group (P <0.05). Conclusion: Continuous stimulation with angiotensin Ⅱ can induce electrical remodeling of ventricular myocytes and may be an important mechanism of ventricular arrhythmia.