THE ROLE OF PHOSPHOLIPASE IN MITOCHONDRIAL DYSFUNCTION AFTER CORONARY REPERFUSION IN THE CANINE MYOCARDIUM
スポンサーリンク
概要
- 論文の詳細を見る
The left anterior descending coronary artery of a dog was occluded for 15 min followed by a 5 min reperfusion in order to investigate the mechanism responsible for the paradoxical exacerbation of heart mitochondrial dysfunction caused by reperfusion. the mitochondrial function was assessed and the concentration of Ca^<++>, phospholipids and free fatty acids (FFA) were determined. The relative importance of mitochondrial lysophospholipids was also investigated. Eleven dogs (30.6%) developed "resperfusion arrhythmia" (arrhythmia group) but 23 did not (control group). Although mitochondrial dysfunction was observed in the reperfused area even in the control group, a greater impairment of mitochondrial function was observed in the reperfused area in the arrhythmia group. There was no significant difference in the contents of FFA and phospholipids in the mitochondria from the normal area of both groups and from the reperfused area of the control group. However, a marked increase in eight FFA and a significant decrease in phospholipids were observed in the mitochondria from the reperfused area of the arrhythmia group. A significant increase in Ca<++> content both in the myocardium and the mitochondria from the reperfused area was observed in the arrhythmia group but not in the control group. In separate experiments, the mitochondria prepared from dog left ventricle were incubated with either phospholipase C (PhC) or phospholipase A_2 (PhA_2). Both phospholipases induced severe mitochondrial dysfunction. PhC induced a significant increase in FFA, quite analogous to the changes in mitochondrial FFA caused by reperfusion in vivo. PhA_2 also induced a tremendous increase in FFA but only in the content of unsaturated FFA. Although PhC did not affect the lysophospholipid profiles, PhA_2 induced lysophosphatidyl choline. These results indicate that mitochondrial damages characteristic of the early phase of coronary reperfusion may be caused by the action of PhC, activated by increased intracellular Ca^<++>, which in turn induces degradation of the mitochondrial membrane.
- 社団法人日本循環器学会の論文
- 1984-05-20
著者
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SUGIYAMA Satoru
Department of Pharmacology, Aichi Medical University School of Medicine
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Ogawa Kouichi
Meijo Hospital
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Ogawa Kouichi
Department of Cardiology, Meijo Hospital
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Satake Tatsuo
Department of Biomedical Chemistry and of Internal Medicine, Faculty of Medicine, University of Nago
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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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Satake T
Departments Of Internal Medicine Faculty Of Medicine University Of Nagoya
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Ozawa Takayuki
Biomedical Chemistry Faculty Of Medicine University Of Nagoya
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Ogawa K
Meijo Hospital
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Shibata T
Nagoya Univ. Nagoya Jpn
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Ogawa Kouichi
Second Department Of Internal Medicine Nagoy University School Of Medicine
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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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Sugiyama Satoru
Biomedical Chemistyry 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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Satake Tatsuo
The 2nd Dept. Of Internal Medicine Nagoya University School Of Medicine
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Miyazaki Yutaka
Department Of Internal 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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Ogawa Kouichi
Department Of Anatomy School Of Medicine Fukuoka University
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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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