Objective: The purpose of the present study was to study the influence of left ventricular myocardial infarction on gap junction protein connexin 40 in the atria, and to observe the intervention function of carvedilol as an adrenergic receptor blocker.
Methods and results: Thirty New Zealand rabbits were randomly divided into three experimental groups: myocardial infarction, carvedilol and control groups. The left anterior descending coronary artery was ligated in animals in the myocardial infarction group; in the control animals no artery was ligated. The animals in the carvedilol group were administered carvedilol by way of gavages at a dose of 0.5 mg/kg. After the experiment had gone on for 8 weeks, the spatial distribution and the amount of gap junction protein connexin 40 in the left auricle ware measured by fluorescence immunohistochemistry and Western blot, respectively. Compared with the controls, the amount of left atrial appendage gap junction protein connexin 40 in the myocardial infarction group was significantly decreased (P < 0.01), and an uneven distribution of gap junction protein connexin 40 was markedly observed. The amount of gap junction protein connexin 40 in the carvedilol group was higher than that in the myocardial infarction group (P < 0.05), and the uneven distribution was minimized in animals with carvedilol administration.
Conclusion: Left ventricular myocardial infarction can cause a remodelling of gap junction protein connexin 40 in the atria, which becomes distributed with a high heterogeneity and is significantly decreased in the amount of protein. Carvedilol can reduce this remodelling of gap junction protein connexin 40.