Neutrophil-induced Myocardial Cell Damage and Active Oxygen Metabolites : 54th Annual Scientific Session of the Japanese Circulation Society
スポンサーリンク
概要
- 論文の詳細を見る
Free radicals derived from polymorphonuclear leukocytes (PMN) have been suggested to play an important role in myocardial ischemia-reperfusion injury. To define the mechanism by which activated PMN exacerbate ischemic myocardial damage. we investigated the extent of cell injury. free radical generation and lipid peroxidation in embryo mouse myocardial cells co-incubated with activated PMN. The generation of free radicals derived from PMN correlated with the extent of myocardial cell injury. Among the cell sheets preconditioned with hypoxic and glucose free medium. PMN-adhered myocardial cells were initially injured after adding PMN activator. extending to adjacent cells. Chemiluminescence emission and thiobarbituric acid reactive substance in the co-incubated cells were markedly increased and sustained compared with those in each cell monoincubation. The augmented lipid peroxidation was related to the progression of myocardial cell injury. These results indicate that PMN-derived free radicals cause membrane disruption, contributing to the progression of myocardial injury.
- 社団法人日本循環器学会の論文
- 1991-11-20
著者
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Minamino Takazo
Department Of Internal Medicine And Therapeutics Osaka University Graduate School Of Medicine
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Kitabatake Akira
Department Of Cardiovascular Medicine Hokkaido University School Of Medicine
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Kitabatake Akira
The First Department Of Medicine Osaka University School Of Medicine
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Kitabatake Akira
From The Division Of Cardiology First Department Of Medicine And The Department Of Pathophysiology O
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Tada Michihiko
大阪大学 医系研究 病理病態
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TADA MICHIHIKO
From the Division of Cardiology, Cardiac Care Unit, Osaka Keisatsu Hospital and the Division of Card
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KUZUYA TSUNEHIKO
From the Division of Cardiology, Cardiac Care Unit, Osaka Keisatsu Hospital and the Division of Card
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Fuji Hisakazu
From The Division Of Cardiology First Department Of Medicine And The Department Of Pathophysiology O
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Arai Kazutaka
First Department Of Medicine And Faculty Of Medical Information Science Osaka University School Of M
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Tada Michihiko
First Department Of Medicine And Department Of Pathophysiology Osaka University School Of Medicine
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HOSHIDA SHIRO
From The Division of Cardiology, First Department of Medicine and The Department of Pathophysiology,
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Mandai Takashi
The Division Of Cardiology Sakurabashi Watanabe Hospital
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Tada Michihiko
1st Department Of Medicine Osaka University Medical School Osaka
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Kitabatake Akira
First Department Of Medicine And Faculty Of Medical Information Science Osaka University School Of M
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Kitabatake Akira
First Department Of Medicine And Faculty Of Medical Information Science Osaka University School Of Medicine
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Kitabatake A
Department Of Cardiovascular Medicine Hokkaido University Graduate School Of Medicine
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