THE EFFECT OF VERAPAMIL ON REPERFUSION ARRHYTHMIA IN CANINE HEART
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概要
- 論文の詳細を見る
This study was designed to clarify the mechanism of reperfusion arrhythmia and with the effect of verapamil on arrhythmia. In vivo study Fifth anesthetized dogs were divided into two groups the control group (n=37) and the verapamil group (n=13). The left anterior descending coronary artery (LAD) was occluded for 15 min and then reperfused for 5 min. Physiological saline or verapamil (0.4 mg/kg) was infused 5 min prior to the LAD reperfusion. Eleven (30%) of the control dogs developed "reperfusion arrhythmia" (arrhythmia group) but 26 did not (non-arrhythmia group), while in the verapamil group, none of the 13 dogs developed arrhythmia. Immediately after 5 min reperfusion, myocardial plasma membrane and mitochondria were prepared from the normal and the reperfused area. In the arrhythmia group, an increase in free fatty acids (FFA) and a decrease in phospholipids were observed in membrane samples, and the content of calcium in the mitochondria increased in the reperfused myocardium; these changes were not observed in the non-arrhythmia group or the verapamil group. In vitro study In vitro study consisted of two experiments. In experiment 1, incubation of myocardial plasma membrane with phospholipase (PLase) A_2 increased only the unsaturated FFA, while PLase C increased all the detected FFA. In experiment 2, the effects on myocardial membrane potentials induced by PLase A_2 and PLase C were studied by using microelectrodes. Each PLase caused a decrease in the resting potential and in the magitude and duration of the action potential. These results and the fact that Ca^<2+> is the essential factor which activates PLase suggest that the activation of PLase, triggered by Ca^<2+> influx associated with reperfusion, develops the arrhythmogenic conditions, and that the protective effect of verapamil is based on inhibiting the activation of PLases by interfering with Ca^<++> influx.
- 社団法人日本循環器学会の論文
- 1985-12-20
著者
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SUGIYAMA Satoru
Department of Pharmacology, Aichi Medical University School of Medicine
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Hattori Masaki
Department of Cardiology, Meijo Hospital
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Ozawa Takayuki
Department of Biomedical Chemistry and of Internal Medicine, Faculty of Medicine, University of Nago
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Nagai Shuichiro
Departments of InternaI Medicine, FacuIty of Medicine, University of Nagoya
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Miyazaki Yutaka
2nd Dept.of Internal Medicine Nagoya University School Of Medicine
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Miyazaki Yutaka
名古屋大学 生化
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Miyazaki Yutaka
Department Of Toxicology Aichi Prefectural Institute Of Public Health
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Hattori Masaki
Department Of Internal Medicine University Of Nagoya
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Hattori Masaki
Department Of Cardiology Meijo Hospital
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Ozawa Takayuki
Biomedical Chemistry Faculty Of Medicine University Of Nagoya
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Sugiyama Satoru
Biomedical Chemistry Faculty Of Medicine University Of Nagoya
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Sugiyama Satoru
Department Of Biomedical Chemistry
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Nagai Shuichiro
Departments Of Internal Medicine And Biomedical Chemistry
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Ozawa Takayuki
Departments Of Biomedical Chemistry Faculty Of Medicine University Of Nagoya
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Ozawa Takayuki
The Department Of Biomedical Chemistry Faculty Of Medicine University Of Nagoya
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Sugiyama Satoru
Biomedical Chemistyry Faculty Of Medicine University Of Nagoya
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Sugiyama Satoru
Departments Of Biomedical Chemistry Faculty Of Medicine University Of Nagoya
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Miyazaki Yutaka
The 2nd Department Of Internal Medicine Nagoya University School Of Medicine
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Ozawa T
The Department Of Biomedical Chemistry Faculty Of Medicine University Of Nagoya
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Miyazaki Yutaka
Department Of Internal Medicine University Of Nagoya
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Sugiyama Satoru
Faculty Of Medicine University Of Nagoya
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Ozawa Takayuki
Department Of Biomedical Chemistry
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Ozawa T
Biomedical Chemistry Faculty Of Medicine University Of Nagoya
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Ozawa Takayuki
Departments Of Biomedical Chemistry University Of Nagoya
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Miyazaki Yutaka
Department of Information Systems Design, Doshisha University, Kyotanabe, Kyoto 610-0321, Japan
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