Sevoflurane postconditioning alleviates action potential duration shortening and L-type calcium current suppression induced by ischemia/reperfusion injury in rat epicardial myocytes  

作　　者：GONG Jun-song YAO Yun-tai FANG Neng-xin HUANG Jian LI Li-huan 

机构地区：[1]Department of Anesthesiology, Fuwai Hospital, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China [2]Department of Pathology and Pathophysiology, Fuwai Hospital, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China

出　　处：《Chinese Medical Journal》2012年第19期3485-3491,共7页中华医学杂志（英文版）

基　　金：This work was supported by the grant Irom the National Natural Science Foundation of China （No. 81070098） and Foundation for Postgraduates＇ Innovative Research of Peking Union Medical College （No. 2010-1002-004）.

摘　　要：Background It has been proved that sevoflurane postconditioning （SpostC） could protect the heart against myocardial ischemia/reperfusion injury, however, there has been few research focused on the electrophysiological effects of SpostC. The objective of the study was to investigate the effects of SpostC on action potential duration （APD） and L-type calcium current （Ica, L） in isolated cardiomyocytes. Methods Langendorff perfused SD rat hearts were randomly assigned to one of the time control （TC）, ischemia/reperfusion （I/R, 25 minutes of ischemia followed by 30 minutes of reperfusion）, and SpostC （postconditioned with 3% sevoflurane） groups. At the end of reperfusion, epicardial myocytes were dissociated enzymatically for patch clamp studies. Results Sevoflurane directly prolonged APD and decreased peak Ica, L densities in epicardial myocytes of the TC group （P〈0.05）. I/R injury shortened APD and decreased peak Ica, L densities in epicardial myocytes of the I/R group （P〈0.05）. SpostC prolonged APD and increased peak Ica, L densities in epicardial myocytes exposed to I/R injury （P〈0.05）. SpostC decreased intracellular reactive oxygen species （ROS） levels, reduced the incidence of ventricular tachycardia and ventricular fibrillation, and decreased reperfusion arrhythmia scores compared with the I/R group （all P〈0.05）. Conclusions SpostC attenuates APD shortening and Ica, L suppression induced by I/R injury. The regulation of APD and lea, L by SpostC might be related with intracellular ROS modulation, which contributes to the alleviation of reperfusion ventricular arrhvthmia.Background It has been proved that sevoflurane postconditioning （SpostC） could protect the heart against myocardial ischemia/reperfusion injury, however, there has been few research focused on the electrophysiological effects of SpostC. The objective of the study was to investigate the effects of SpostC on action potential duration （APD） and L-type calcium current （Ica, L） in isolated cardiomyocytes. Methods Langendorff perfused SD rat hearts were randomly assigned to one of the time control （TC）, ischemia/reperfusion （I/R, 25 minutes of ischemia followed by 30 minutes of reperfusion）, and SpostC （postconditioned with 3% sevoflurane） groups. At the end of reperfusion, epicardial myocytes were dissociated enzymatically for patch clamp studies. Results Sevoflurane directly prolonged APD and decreased peak Ica, L densities in epicardial myocytes of the TC group （P〈0.05）. I/R injury shortened APD and decreased peak Ica, L densities in epicardial myocytes of the I/R group （P〈0.05）. SpostC prolonged APD and increased peak Ica, L densities in epicardial myocytes exposed to I/R injury （P〈0.05）. SpostC decreased intracellular reactive oxygen species （ROS） levels, reduced the incidence of ventricular tachycardia and ventricular fibrillation, and decreased reperfusion arrhythmia scores compared with the I/R group （all P〈0.05）. Conclusions SpostC attenuates APD shortening and Ica, L suppression induced by I/R injury. The regulation of APD and lea, L by SpostC might be related with intracellular ROS modulation, which contributes to the alleviation of reperfusion ventricular arrhvthmia.

关 键 词：SEVOFLURANE POSTCONDITIONING ISCHEMIA/REPERFUSION L-type calcium current 

分 类 号：X[环境科学与工程]