Effects of different concentrations of remifentanil on expression and distribution of gap junction protein connexin 43 in cardiomyocytes of rabbits
10.3760/cma.j.issn.0254-1416.2016.03.015
- VernacularTitle:不同浓度瑞芬太尼对兔心肌细胞缝隙连接蛋白43表达及分布的影响
- Author:
Yanqiu LIU
;
Kaiqiang ZHANG
;
Hui LI
;
Hong GAO
;
Yonghong XIONG
- Publication Type:Journal Article
- Keywords:
Piperidines;
Connexin 43;
Myocytes,cardiac
- From:
Chinese Journal of Anesthesiology
2016;36(3):311-313
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effects of different concentrations of remifentanil on the expression and distribution of gap junction protein connexin 43 (Cx43) in the cardiomyocytes of rabbits.Methods Healthy adult rabbits of both sexes,weighing 2.0-2.5 kg,were anesthetized with pentobarbital sodium.Their hearts were rapidly excised and retrogradely perfused in a Langendorff apparatus with K-H solution saturated with 95％ O2-5％ CO2 at 37 ℃.After 15 min of stabilization with K-H solution,the 24 isolated hearts were randomly divided into 4 groups (n =6 each) using a random number table:control group (group C),and low,medium and high concentrations of remifentanil groups (R1-3 groups).The hearts were continuously perfused with K-H solution at 37 ℃ in group C.The hearts were perfused for 60 min with K-H solution containing remifentanil 12,25 and 50 ng/ml in R1-3 groups,respectively.The myocardial specimens were then obtained from the anterior wall of the left ventricle for detection of the expression and distribution of Cx43 by Western blot and immunohistochemistry,respectively.Results The expression of Cx43 was gradually down-regulated in C and R1-3 groups in turn (P＜0.05).Compared with group C,there was a tendency for the proteins localized at end-to-end contact sites of ventricular cardiomyocytes to localize at side-to-side contact sites in R1-3 groups,and the distribution was messy in R1-3 groups.Conclusion Remifentanil dose-dependently down-regulates the expression of Cx43 and changes the distribution of Cx43,which may be one of the mechanisms of remifentanil-induced arrhythmia in rabbits.
