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Title:
To Explore the Mechanism of Benazepril in Upstream Treatment for Arrhythmia Preventing the Degradations of Cx43, Cx40
Authors:  Dabin Pan, M.D., Wenlong Ding, M.M., Jiming Chen, M.M., and Zeyang Shan, M.M.
  Objective: Arrhythmia is a fatal risk factor. Traditional antiarrhythmic drugs may cause arrhythmia. Diabetic cardiomyopathy is one of the causes of arrhythmia. Angiotensin converting enzyme inhibitors are one of the possible drugs to prevent arrhythmia. Connexin 43 and connexin 40 are important pathogenic links of arrhythmia. The aim of this study was to investigate whether benazepril affects the expression of connexin 43 and connexin 40.
Study Design:
Sprague Dawley rats were randomly divided into normal control group, diabetes group, and benazepril-treated diabetes group. ECG was recorded to detect PR interval, QTc interval, and QTc dispersion. Weight and heart weight of rats were recorded. The arrangement of myocardium was observed by immunohistochemistry. The density of connexin 43 was detected by immunofluorescence, and the expressions of connexin 43, pcx43, and connexin 40 were detected by western blot.
Results:
Compared with the normal control group, the body weight and heart weight of the diabetic group were significantly reduced, but the ratio of heart weight to body weight was significantly increased, the PR interval, QTc interval, and QTc dispersion were significantly prolonged (p<0.01 or p<0.05), the incidence of arrhythmia was significantly increased (p<0.01), the expression of connexin 43 and connexin 40 was significantly decreased (p<0.05), and the expression of connexin 43 was significantly decreased (p<0.01). Benazepril can significantly improve or prevent the above pathological changes in diabetic rats (p<0.01 or p<0.05).
Conclusion:
Benazepril inhibits the degradation of Cx43 and pcx43 in diabetic rats, which may be one of the mechanisms of benazepril upstream in the treatment of arrhythmia.
Keywords:  arrhythmia, benazepril, connexin, diabetes, myocardium
   
   
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