Dipyridamole Suppresses Catecholamine-and Ca⁺⁺ Influx-Sensitive Ventricular Arrhythmias

• Kobayashi Youichi

  The Third Department of Internal Medicine, Showa University School of Medicine

• Miyata Akira

  The Third Department of Internal Medicine, Showa University School of Medicine

• Chiyoda Kazumi

  The Third Department of Internal Medicine, Showa University School of Medicine

• Nakagawa Haruyuki

  The Third Department of Internal Medicine, Showa University School of Medicine

• Jinbo Yoshihiro

  The Third Department of Internal Medicine, Showa University School of Medicine

• Tanno Kaoru

  The Third Department of Internal Medicine, Showa University School of Medicine

• Kikushima Shuji

  The Third Department of Internal Medicine, Showa University School of Medicine

• Kurano Kozo

  The Third Department of Internal Medicine, Showa University School of Medicine

• Baba Takao

  The Third Department of Internal Medicine, Showa University School of Medicine

• Katagiri Takashi

  The Third Department of Internal Medicine, Showa University School of Medicine

抄録

To study the mechanism of ventricular arrhythmias, the effect of dipyridamole (DIP; 300 mg/day), an adenosine transport inhibitor, on ventricular premature contractions (VPCs) was assessed in 12 patients who showed VPCs (21312±12314/day) on Holter ECG in a controlled setting. The effects were compared with those of verapamil (240 mg/day) and bisoprolol (5 mg/day). DIP suppressed more than one-half the VPCs in 5 patients. The mean degree of reduction in these DIP-responders was 75±18%. Both verapamil and bisoprolol inhibited VPCs in all of the DIP-responders (verapamil: 71±15%, bisoprolol: 88±16%). Two of the 5 DIP-responders had sustained ventricular tachycardias (VT) that were terminated by intravenous DIP, ATP, acetylcholine, verapamil, and propranolol. In contrast, verapamil did not inhibit VPCs in any of the DIP-nonresponders. Bisoprolol also did not suppress VPCs in 3 of 6 DIP-non responders. Heart rate was unaffected by DIP, but was suppressed by both verapamil and bisoprolol. In addition, DIP increased the serum concentration of adenosine (control 16.3 ±17.1 vs 22.3±19.0 pmol/ml after DIP, p<0.05). The inhibitory effect of DIP may involve suppression of Ca⁺⁺ current through an extracellular increase in adenosine. (Jpn Circ J 1996; 60: 629 - 640)

収録刊行物

• JAPANESE CIRCULATION JOURNAL

  JAPANESE CIRCULATION JOURNAL 60 (9), 629-640, 1996

  社団法人 日本循環器学会

キーワード

• Dipyridamole
• Ventricular arrhythmia
• Adenosine
• Verapamil
• Triggered activity

詳細情報

• CRID: 1390001206428625664
• NII論文ID: 110002560995
• NII書誌ID: AA00690731
• DOI: 10.1253/jcj.60.629
• COI: 1:CAS:528:DyaK28XntlGrtL4%3D
• ISSN: 13474839
• ISSN: 00471828
• PubMed: 8902581
• Web Site: http://www.jstage.jst.go.jp/article/jcj/60/9/60_9_629/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/1997060213
• 本文言語コード: en
• データソース種別:
  • JaLC
  • Crossref
  • PubMed
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可