Effects of remifentanil post-conditioning on aquaporin-1 expression during myocardial ischemia-reperfusion injury in rats
10.3760/cma.j.issn.0254-1416.2014.09.027
- VernacularTitle:瑞芬太尼后处理对大鼠心肌缺血再灌注损伤时水通道蛋白1表达的影响
- Author:
Zhongmeng LAI
;
Hong ZHENG
;
Wenhua CHEN
;
Liangcheng ZHANG
;
Pengtao LIN
- Publication Type:Journal Article
- Keywords:
Piperidines;
Myocardial reperfusion injury;
Aquaporin 1
- From:
Chinese Journal of Anesthesiology
2014;34(9):1128-1130
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effects of remifentanil post-conditioning on aquaporin-1 (AQP-1) expression during myocardial ischemia-reperfusion (I/R) injury in rats.Methods Twenty-four male.SpragueDawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =8 each) using a random number table:sham operation group (group S),group I/R,and remifentanil post-conditioning group (group RP).Myocardial I/R was induced by 45 min occlusion of left anterior descending branch of coronary artery followed by 24 h reperfusion.Remifentanil 10 μg· kg-1· min-1 was infused over 10 min starting from 10 min before reperfusion in group RP,while the equal volume of normal saline was given instead in S and I/R groups.At the end of reperfusion,all the rats were sacrificed and their myocardial specimens from left ventricles were obtained for microscopic examination of thepathological changes and for determination of AQP-1 mRNA (using real-time fluorescent quantitative PC R) and AQP-1 protein (by Western blot) expression in the ischemic area and myocardial water content.Results Compared with S group,myocardial water content was significantly increased in the other two groups,AQP-1 mRNA and protein expression was up-regulated in group I/R,and no significant change was found in AQP-1 mRNA and protein expression in RP group.Compared with I/R group,myocardial water content was significantly reduced,and AQP-1 mRNA and protein expression was down-regulated in RP group.Conclusion Remifentanil post-conditioning reduces myocardial I/R injury possibly through down-regulating AQP-1 expression in myocardial tissues of rats.
