ANTIARRHYTHMIC EFFECTS OF EICOSAPENTAENOIC ACID DURING MYOCARDIAL INFARCTION : Enhanced Cardiac Microsomal(Ca^<2+>-Mg^<2+>)-ATPase Activity
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概要
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The effects of dietary supplementation with eicosapentaenoic acid (EPA) on ventricular arrhythmias during myocardial infarction were examined in a canine model. EPA was incorporated into cellular membranes after ingestion of EPA-ester (100 mg/kg body weight/day) for 8 weeks. The ratio of EPA to arachidonic acid (AA) in platelet cell membranes and myocardial microsomes was significantly increased (7% to 37% in platelet cell membranes; p<0.01, 3% to 12% in non-infarcted cardiac microsomes; p<0.01, and from 2% to 8% in infarcted cardiac microsomes; p<0.01). Dietary supplementation with EPA significantly reduced the incidence and severity of arrhythmias during coronary artery occlusion. Immediately after coronary artery occlusion, all of the animals in the control group that were given a toxic dose of digitalis developed ventricular tachycardia (VT) or ventricular fibrillation (Vf) , whereas none of the animals in the EPA-supplement group developed VT or Vf within 15 min after administration of digitalis. Regardless of the presence of an infarcted area, the specific activity of the Ca^<2+>-pump enzyme ((Ca^<2+>-Mg^<2+>)-ATPase) within the myocardial microsomal fraction of the EPA-supplemented group was significantly higher than in that of the control group (Vmax: 140.5±19.1 vs 94.8±28.9 nmol/mg/min in non-infarcted cardiac microsomes, p<0.01, 130.9±18.4 vs 90.2±26.4 nmol/mg/min in infarcted cardiac microsomes, p<0.01, EPA vs control group, respectively) . The specific activities of the Na^+-pump enzyme ((Na^+-K^+)-ATPase) and NADPH-dependent cytochrome C reductase in infarcted and non-infarcted cardiac microsomes did not differ between these groups. These results indicate that EPA supplementation increases the (Ca^<2+>-Mg^<2+>)-ATPase activity within myocardial membranes that is involved in Ca^<2+> metabolism in myocardial cells by increasing the ratio of EPA to AA within cellular membranes. These cellular alterations are likely to reduce the severity of ventricular arrhythmias by inhibiting the rapid accumulation of intracellular Ca^<2+> following ischemia.
- 社団法人日本循環器学会の論文
- 1994-11-20
著者
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Kinoshita Isao
Department Of Biology Faculty Of Science Nara Women Is University:(present)bio-resources Technology
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Kinoshita Isao
Department Of Cardiology The Center For Adult Diseases
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Hirota Hisao
Department Of Cardiology The Center For Adult Diseases
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ITOH Kazuyuki
Department of Biology, Osaka Medical Center for Cancer and Cardiovascular Diseases
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Otsuji Satoru
Department Of Cardiology The Center For Adult Diseases
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Otsuji Satoru
Department Of Cardiology Osaka Medical Center For Cancer And Cardiovascular Diseases
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Shibata Nobuhiko
Department Of Cardiology The Center For Adult Diseases
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NISHIDA-NAKAI MARIKO
Department of Cardiology, The Center for Adult Diseases
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Nishida-nakai Mariko
Department Of Cardiology The Center For Adult Diseases
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Itoh Kazuyuki
Department Of Biology Osaka Medical Center For Cancer And Cardiovascular Diseases
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Itoh Kazuyuki
Department Of Cardiology The Center For Adult Diseases
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SHIBATA NOBUHIKO
Department of Cardiology, The Center for Adult Diseases
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