Effect of anisodamine on myocardial connexin 43 expression in pig after resuscitation from cardiac arrest
10.3760/cma.j.issn.2095-4352.2015.03.010
- VernacularTitle:山莨菪碱对心搏骤停复苏猪心室肌缝隙连接蛋白43表达的影响
- Author:
Yahua LIU
;
Hong SHEN
;
Lixiang WANG
;
Huining YANG
;
Lizhi MA
- Publication Type:Journal Article
- Keywords:
Ventricular fibrillation;
Cardiopulmonary resuscitation;
Anisodamine;
Connexin 43
- From:
Chinese Critical Care Medicine
2015;31(3):209-212
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the effect of anisodamine on the expression of connexin 43 (Cx43) in swine ventricular myocardium after resuscitation from cardiac arrest.Methods The experiment was conducted on healthy pigs, and they were randomly divided into three groups, namely sham group, epinephrine group (control group) and anisodamine group (experimental group, animals were resuscitated combined with injection of 0.4 mg/kg of anisodamine), with 5 pigs in each group. Model of ventricular fibrillation was reproduced by alternating current challenge, and cardiopulmonary resuscitation (CPR) was performed 8 minutes after cardiac arrest. Left ventricular myocardium was harvested at 24 hours after restoration of spontaneous circulation. The expression and distribution of Cx43 were observed by immunofluorescence, Cx43 mRNA expression was assessed with reverse transcription-polymerase chain reaction (RT-PCR), and the protein expressions of Cx43 and phosphorylation of Cx43 (p-Cx43) were analyzed by Western Blot.Results The positive expression of Cx43 in ventricular muscle was distributed uniformly, mostly at the end-to-end linkage of myocardial cells, with a few side-to-side linkage in sham group. The positive expression of Cx43 in control group was significantly weaker than that in the sham group, and the signal intensity was significantly declined (4.35±2.10 vs. 10.02±3.66,P< 0.01). The positive expression of Cx43 at the end-to-end linkage and side-to-side linkage was irregular in experimental group, and the signal intensity was obviously higher than that in the control group (7.91±2.54 vs. 4.35±2.10,P< 0.05), but it was significantly weaker than that in the sham group (7.91±2.54 vs. 10.02±3.66,P< 0.05). For control group and experimental group, the Cx43 mRNA and protein expressions were significantly lower than those of the sham group [Cx43 mRNA (A value): 0.32±0.05, 0.32±0.03 vs. 0.48±0.07; Cx43 protein (A value): 0.43±0.03, 0.50±0.07 vs. 0.65±0.04, allP< 0.01], and there were no significant differences between experimental group and control group (allP> 0.05). The p-Cx43 protein expression of control group was significantly lower than that of the sham group (A value: 0.22±0.03 vs. 0.37±0.06,P< 0.01), and it was significantly higher in the experiment group than that in the control group (A value: 0.29±0.07 vs. 0.22±0.03, P< 0.01), but there was no significant difference with the sham group (P> 0.05). No significant difference in p-Cx43/Cx43 was found among sham, control, and experiment groups (0.57±0.09, 0.51±0.05, 0.58±0.06, all P> 0.05).ConclusionAnisodamine can improve the abnormal expression of Cx43 in ventricular muscle of pigs with cardiac arrest, which may be related to the protection effect of anisodamine on cardiac conduction.
