Effects of Ang II perfusion on transmural heterogeneous of Cx43 in acute myocardial ischemia reperfusion
10.1016/j.apjtm.2015.12.019
- Author:
Xiao-Pan CHEN
1
;
Zheng-Wang LIU
1
;
Shi-Juan LU
2
;
Kang HUANG
2
;
Wei ZHANG
2
;
Jiang-Hua ZHONG
2
Author Information
1. Hainan Medical University Affiliated Hospital
2. Central South University Xiangya School of Medicine Affiliated Haikou Hospital, Haikou People's Hospital
- Publication Type:Journal Article
- Keywords:
Acute myocardial ischemia reperfusion;
Angiotensin II;
Cx43;
Dispersion of repolarization
- From:
Asian Pacific Journal of Tropical Medicine
2016;9(1):96-99
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To observe the effects of angiotensin II(Ang II) perfusion on transmural heterogeneity of Cx43 expression in the rabbit model with acute myocardial ischemia reperfusion (MIR), and investigate the role of rennin-angiotensin system in malignant ventricular arrhythmia induced by MIR. Methods: Twenty rabbits were randomly divided into MIR group (n = 10) and Ang II group (n = 10). MIR model was produced with traditional ligation and opening of the anterior descending coronary artery in all animal. The hearts in vitro in the MIR group and the Ang II group were perfused with simply improved Tyrode's solution and containing Ang II Tyrode's solution respectively. 90% monophasic action potential repolarization duration, transmural dispersion of repolarization, Cx43 protein (Cx43-pro) and mRNA (Cx43-Cq) expression in subepicardial, midmyocardial and subendocardial myocardium were measured in both groups. The greatest differences of Cx43-pro and Cx43-Cq among three myocardial layers were calculated and shown with ΔCx43-pro and ΔCx43-Cq respectively. Results: After Ang II perfusion, 90% monophasic action potential repolarization duration among three myocardial layer were significantly prolonged (P < 0.05 and P < 0.01), and transmural dispersion of repolarization also significantly increased compared with the MIR group (P < 0.05). Compare with the MIR group, three myocardial Cx43-pro and Cx43-Cq expression in the Ang II group were significantly decreased (P < 0.05 and P < 0.01), but ΔCx43-pro and ΔCx43-Cq were significant increased. Conclusions: Renin-angiotensin system increases transmural heterogeneity of Cx43 expression in the rabbit model with MIR by Ang II, and enlarge transmural dispersion of repolarization among three myocardial layers of left ventricular which induces malignant ventricular arrhythmia.
