1994 Fiscal Year Final Research Report Summary
New myocardial motection with cytokine network.
| Project/Area Number |
05454386
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Thoracic surgery
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| Research Institution | Osaka University |
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Principal Investigator |
NAKANO Susumu Osaka University Medical Lecturer, 医学部, 講師 (70028653)
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| Co-Investigator(Kenkyū-buntansha) |
SAWA Yoshiki Osaka University Medical Assitant, 医学部, 助手 (00243220)
KADOBA Keishi Osaka University Medical Assitant, 医学部, 助手 (00185886)
NAKATA Seizo Osaka University Medical Assitant, 医学部, 助手 (50116068)
SHIRAKURA Ryota Osaka University Medical Professor, 医学部, 教授 (00116047)
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| Project Period (FY) |
1993 – 1994
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| Keywords | Reperfusion / Neutrophil / Cytokine / Myocyte / Endothelial cell / Adhesion / Migration / Free radical |
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| Research Abstract |
To elucidate the mechanism of neutrophil(Np) induced reperfusion injury in myocardium, Np myocytes(Mc) and endothelial cells(Ec) were isolated from adult rat heart and blood. To elucidate the hypothesis that Np plays a role in reperfusion injury, a coincubation system with a monolayr of endothelial cells on the collagen membrane and myocytes under a collagen membrane was established. In this system, significant increase of Np migration through Ec, Mc damage and count of chemiluminescence were increased by 2 hours of hypoxia.However, these changes were decreased by administration of monoclonal antibody anti ICAM-1 and IL-6. Hypoxic Mc and Ec showed significant expression of ICAM-1. In the supernatant of hypoxic myocyte, significant increase of IL-6 was detected as compared to normoxic myocytes. These results suggested that ICAM-1 on Ec and Mc is implicated in Np migration through Ec and Np induced damage resulting in the extension of reperfusion injury in myocardium. Moreover, IL-6 may be derived from hypoxic myocytes and promote neutrophil induced reperfusion injury.
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