Effects Of β-acceptor Blocker On Connexin 43 Of Myocardial Gap Junction After Acute Ischemia Injury

Objectives The aim of the study was to observe the effects ofβ-acceptor blocker on Connexin 43 in order to make clear the protective mechanism against ischemia-induced arrhythmias.Methods The rats were randomly divided into 4 groups: sham operation group(SM group, n=8), ischemia group(IM group,n=8),metoprolol group(MTP group,n=8),carvedilol group(CVD group,n=8). Metoprolol(6mg/kg/d) was given intragastrically in MTP group, carvedilol (3mg/kg/d) was given intragastrically in CVD group,and equal normal saline was given in SM group and IM group for seven days. Then ligated the left anterior descending coronary artery for 60 minutes to build ischemia injury model in IM,MTP and CVD group,and braided the left anterior descending coronary artery in SM group. After 60 minutes ischemia,the expression of Connexin 43 of the ischemic myocardium was studied by immunohistochemistry technique. The ventricular arrhythmia were observed and MDA ,SOD were measured. The tissue samples of the infarcted areas were examined by electron microscope.Results1,VAS and concentration of MDA increase obviously and activity of SOD degrade in rats of IM group,as Compared with SM group (P<0.01) ,there is significant difference, the expression of Cx43 is evidently decreased and the distribution is disturbed,and the Ultrastructure of ventricular myocardium was abnormal in IM group.2,Carvedilol and Metoprolol obviously decreased the VAS caused by ischemia (P<0.01), increased the activity of SOD, inhibited the reduction in MDA content of serum, and resulted in normal distribution and content of Cx43. Compared with IM group,the changes of heart ultrastucture ameliorated greatly in CVD and MTP group,but couldn't recover to normal state.3,In the CVD group, VAS and content of MDA decrease obviously and activity of SOD raise up (P<0.01), content of Cx43 were significantly higher (P<0.01) ,the distribution pattern of Cx43 was homogeneous and less injury of ultramicrostruture compared with MTP group.Conclusion1,The expression of Cx43 was evidently decreased and the distribution pattern was disturbed in the early stage of acute myocardial ischemia,which could be related to acute Mi-induced arrhythmogenic properties.2,Metoprolol and Carvedilol exerts antiarrhythmogenic effects accompanied by prevention of the loss of Cx43 during acute MI and thus plays a critical role in improving ischemia-induced electrical instability.3,Carvedilol is comparatively more effective among the total, mechanism of this effect is associated with resisting oxidative stress andα₁-acceptor blockage.4,It is most likely that metoprolol and carvedilol protect the rat ischemic ventricular myocytes from injury through the preserved Cx43.