Effects of the Antianginal Drug Trapidil on Atrioventricular Conduction Disturbances During Acute Myocardial Ischemia
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- Watanabe Ichiro
- Division of Cardiology, Department of Medicine, Nihon University School of Medicine
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- Okumura Yasuo
- Division of Cardiology, Department of Medicine, Nihon University School of Medicine
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- Nagashima Koichi
- Division of Cardiology, Department of Medicine, Nihon University School of Medicine
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- Kofune Masayoshi
- Division of Cardiology, Department of Medicine, Nihon University School of Medicine
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- Ohkubo Kimie
- Division of Cardiology, Department of Medicine, Nihon University School of Medicine
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- Mano Hiroaki
- Division of Cardiology, Department of Medicine, Nihon University School of Medicine
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- Sonoda Kazuyuki
- Division of Cardiology, Department of Medicine, Nihon University School of Medicine
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- Kasamaki Yuji
- Division of Cardiology, Department of Medicine, Nihon University School of Medicine
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- Hirayama Atsushi
- Division of Cardiology, Department of Medicine, Nihon University School of Medicine
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抄録
Adenosine and related compounds have been shown to produce atrioventricular (AV) conduction block during acute myocardial ischemia. We investigated the effects of the antianginal drug trapidil, which has been shown to inhibit phosphodiesterase, on AV conduction disturbances in a canine model of acute myocardial ischemia. In 35 anesthetized dogs, the AV node artery was cannulated and perfused with arterial blood. Adenosine (300 μg, 650 μg, or 1000 μg) was injected into the AV node artery. With administration of adenosine at 300 μg, 650 μg, or 1000 μg, the atrio-His (AH) interval was increased by 14.6 ms, 22.3 ms, and 29.7 ms, respectively. The effects of adenosine were potentiated by pretreatment with intravenous dipyridamole (250 μg/kg), an inhibitor of adenosine uptake, but the effects of adenosine were attenuated with intravenous trapidil (3 mg/kg), an inhibitor of phosphodiesterase. AV node artery occlusion resulted in prolongation of the AH interval in 4 of 12 dogs. The ischemia-induced AH prolongation was potentiated with intravenous dipyridamole and attenuated with intravenous trapidil. AV conduction disturbances associated with inferior myocardial infarction may be related in part to endogenously released adenosine, and trapidil may be useful in treating AV block associated with acute AV node ischemia.
収録刊行物
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- International Heart Journal
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International Heart Journal 53 (3), 187-192, 2012
一般社団法人 インターナショナル・ハート・ジャーナル刊行会