Carvedilol Ameliorates the Decreases in Connexin 43 and Ventricular Fibrillation Threshold in Rats with Myocardial Infarction

• Wen Huazhi

  Department of Cardiology, Renmin Hospital of Wuhan University

• Jiang Hong

  Department of Cardiology, Renmin Hospital of Wuhan University

• Lu Zhibing

  Department of Cardiology, Renmin Hospital of Wuhan University

• He Bo

  Department of Cardiology, Renmin Hospital of Wuhan University

• Hu Xiaorong

  Department of Cardiology, Renmin Hospital of Wuhan University

• Chen Jing

  Department of Cardiology, Renmin Hospital of Wuhan University

• Zhao Dongdong

  Department of Cardiology, Renmin Hospital of Wuhan University

抄録

Connexin 43 (Cx43) is the most prominent connexin in the mammalian ventricular myocardium and forms gap junctions that are essential for normal conduction of action potential. Carvedilol, a nonselective β-blocker, is widely used to prevent ventricular arrhythmias after myocardial infarction (MI). Here, we examined the effect of carvedilol on the expression of Cx43 protein and ventricular fibrillation threshold (VFT) using a rat MI model. VFT is defined as the lowest voltage, at which ventricular fibrillation is induced by electrical stimulation. Adult male Wister rats were divided into sham-operated group (n = 20) and MI groups treated with intragastric administration of saline (control, n = 30) or carvedilol (2.5 mg/kg, n = 30) twice a day for 7 days immediately after ligation of the left coronary artery. Compared with sham group (100%), total Cx43 protein and phosphorylated Cx43 protein were decreased in the MI rats to 60 ± 21% and 52 ± 19% (both P < 0.05), respectively. Treatment with carvedilol prevented the MI-induced decrease in total and phosphorylated Cx43 levels (91 ± 17% and 80 ± 20%, both P < 0.05), respectively, which were similar to the levels of sham animals. Moreover, the MI rats exhibited a marked decrease in VFT compared with the sham group (7.2 ± 1.30 vs. 13.0 ± 2.12 V, P < 0.05), but the decrease was abolished by carvedilol (11.0 ± 2.65 V). In conclusion, carvedilol might prevent the ischemia-induced ventricular arrhythmias by restoring Cx43 protein and VFT to the basal levels.

収録刊行物

• The Tohoku Journal of Experimental Medicine

  The Tohoku Journal of Experimental Medicine 218 (2), 121-127, 2009

  東北ジャーナル刊行会

キーワード

• Gap junctions
• connexin43
• phosphorylation
• arrhythmias
• myocardial infarction

詳細情報

• CRID: 1390282679218642560
• NII論文ID: 10025106318
• NII書誌ID: AA00863920
• DOI: 10.1620/tjem.218.121
• ISSN: 13493329
• ISSN: 00408727
• Web Site: http://www.jstage.jst.go.jp/article/tjem/218/2/218_2_121/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2009325507
• 本文言語コード: en
• データソース種別:
  • JaLC
  • Crossref
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可