Item type |
学術雑誌論文 / Journal Article(1) |
公開日 |
2013-08-27 |
タイトル |
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タイトル |
ARRHYTHMIA AFTER THE RELEASE OF INHIBITED OXIDATIVE PHOSPHORYLATION |
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言語 |
en |
言語 |
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言語 |
eng |
キーワード |
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主題 |
Delayed afterdepolarization |
キーワード |
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主題 |
Triggered activity |
キーワード |
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主題 |
Ca2+overload |
キーワード |
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主題 |
Sodium cyanide |
キーワード |
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主題 |
Oxidative phosphorylation |
キーワード |
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主題 |
After comtroction |
キーワード |
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主題 |
Reoxygenation |
資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
その他のタイトル |
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その他のタイトル |
The 53th Annual Scientific Session of the Japanese Circulation Society |
著者 |
Hayashi, Hideharu
Terada, Hajime
Kobayashi, Akira
Yamazaki, Noboru
Terence, F. Mcdonald
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書誌情報 |
Japanese Circulation Journal
巻 54,
号 6,
p. 653-661,
発行日 1989-07-05
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出版者 |
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出版者 |
日本循環器学会 |
権利 |
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権利情報 |
Copyright日本循環器学会 |
権利 |
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権利情報 |
本文データは学協会の許諾に基づきJournal Archiveから複製したものである |
抄録 |
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内容記述タイプ |
Abstract |
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内容記述 |
Automaticities due to delayed afterdepolarizations. elicited upon reoxygenation, are thought to be caused by Ca overload. Since tissue Ca uptake upon reoxygenation has been reported to be closely related to metabolic inhibition during hypoxic perfusion. the relationship between the degree of metabolic inhibition during hypoxia and reoxygenation-induced arrhythmias was investigated in guinea pig papillary muscles. (1) Arrhythmias occurred after 60 min substrate-free hypoxia. but not after 30 min hypoxia. The chance of automaticities was closely related with the increase in resting tention achieved during hypoxic period. The incidence of arrhythmias was. however. lower after 90 or 120 min hypoxia. (2) There were arrhythmias after 20-30 min hypoxia with glycolytic inhibition (20 mM 2-deoxyglucose + 5 mM acetate). On the other hand. 60-min hypoxia in the presence of 5 mM glucose did not elicit arrhythmias on reoxygenation. (3) Stimulation of glycolysis (50 mM glucose) during substrate-free hypoxia prolonged the action potential duration. but did not cause arrhythmias. Washout of cyanide (1 mM) after 60 min perfusion in the presence of oxygen, caused arrhythmias and aftercontractions. These results suggest that the degree of metabolic inhibition during hypoxia is closely related to Ca overload and the resultant arrhythmias upon reoxygena-tion. The release of inhibited oxidative phosphoryiation, rather than the reintroduction of oxygen per se, was thought to be the key mechanism of reoxygenation-induced arrhythmias. |
ISSN |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
00471828 |
EISSN |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
13474839 |
出版社DOI |
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関連タイプ |
isIdenticalTo |
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識別子タイプ |
DOI |
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関連識別子 |
10.1253/jcj.54.653 |
著者版フラグ |
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出版タイプ |
VoR |
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出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |