1987 Fiscal Year Final Research Report Summary
Altered arachidonate lipoxygenase metabolism in reperfused ischemic myocardium.
| Project/Area Number |
61570414
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Osaka University |
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Principal Investigator |
KUZUYA Tsunehiko Assistant Professor, Osaka University School of Medicine, 医学部, 助手 (80150340)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUDA Hisao Resedent, Osaka University School of Medicine, 医学部附属病院, 医員 (30229489)
HOSHIDA Shiro Resident, Osaka University School of Medicine, 医学部附属病院, 医員 (80238732)
KADOMA Masaaki Resident, Osaka University School of Medicine, 医学部附属病院, 医員
TADA Michihiko Professor, Osaka University School of Medicine, 医学部, 教授 (90093434)
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| Project Period (FY) |
1986 – 1987
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| Keywords | Reperfused ischemic myocardium / Arachidonate lipoxygenase metabolism / Neutrophil function / リポキシゲナーゼ代謝阻害剤 |
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| Research Abstract |
To assess the role of neutrophils and arachidonate metabolites in evolving myocardial infarction, we examined the effect of inhibitors of arachidonate metabolism on the extent of myocardial damage and neutrophil function in a 90 minute occlusion-5 hour reperfusion model of canine myocardial infarction. A thromboxane A_2 synthetase inhibitor, CV-4151, and a lipoxygenase inhibitor, AA-861, markedly reduced the infarct size. They also attenuated the production of chemoattractant leukotriene B_4 and chemotactic activity of neutrophils isolated from peripheral circulation. Under these conditions, both the increases in peripheral leukocyte count and neutrophil infiltration in ischemic myocardium were inhibited. These results indicate that the inhibition of two pathways of arachidonate metabolism may decrease infiltration of activated neutrophils in ischemic myocardium by attenuating chemotactic function of neutrophils, resulting in reduction of the extent of myocardial infarction.
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