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Ion mechanism of isoproterenol on delayed afterdepolarization and triggered activity in the infarcted ventricle
Authors:Jin-Liao Gao  Hong-Juan Wang  Yun-Feng Lan  Zhou Fang  Yan Liu  Min Lin  Yi-Cheng Fu  Yang Li
Affiliation:Institute of Geriatric Cardiology, Chinese PLA General Hospital Beijing 100853, China;Institute of Geriatric Cardiology, Chinese PLA General Hospital Beijing 100853, China;Institute of Geriatric Cardiology, Chinese PLA General Hospital Beijing 100853, China;Institute of Geriatric Cardiology, Chinese PLA General Hospital Beijing 100853, China;Institute of Geriatric Cardiology, Chinese PLA General Hospital Beijing 100853, China;Institute of Geriatric Cardiology, Chinese PLA General Hospital Beijing 100853, China;Institute of Geriatric Cardiology, Chinese PLA General Hospital Beijing 100853, China;Institute of Geriatric Cardiology, Chinese PLA General Hospital Beijing 100853, China
Abstract:Objectives This study aimed at investigating the cellular mechanism of isoproterenol (ISO) on delayed afterdepolarizations (DADs) and triggered activity (TA) of the noninfarcted myocardium in the myocardial infarcted rabbit model.Methods Rabbits with the left anterior descending coronary artery occlusion were prepared and recovered for 8 wk (healed myocardial infarction, HMI). Myocytes were isolated from regions of the noninfarcted left ventricular free wall. ISO was added to cellular surface by perfusion way. Action potentials and ion currents were recorded with whole-cell patch clamp. Results The results showed that treatment with ISO induced more DADs and TA events in HMI myocytes. Iti and ICa-L of myocytes treated with ISO were increased significantly compared with HMI cells, which contributed to DADs-related triggered arrhythmia. Conclusions The results suggested that more arrhythmia events of DADs and TA developed in myocytes with ISO treatment. The underlying mechanism was associated with the augment of Iti and calcium influxing (J Geriatr Cardiol 2010; 7:180-183).
Keywords:isoproterenol   healed myocardial infarction   delayed afterdepolarization   triggered activity   ion channels
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