1996 Fiscal Year Final Research Report Summary
ACUTELUNG INJURY INDUCED BY HYPOXA IN RATS
| Project/Area Number |
07671448
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Thoracic surgery
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| Research Institution | Tohoku University |
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Principal Investigator |
ONO Sadafumi Insitute of Development, Aging and Cancer, Tohoku University Department of Thoracic Surgery, Assistant Professor, 加齡医学研究所, 助手 (80250827)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIMURA Shigefumi Insitute of Development, Aging and Cancer, Tohoku University Department of Thora, 加齡医学研究所, 教授 (40006078)
TANITA Tatsuo Institute of Development, Aging and Cancer, Tohoku University Department of Thor, 加齡医学研究所, 助手 (20217144)
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| Project Period (FY) |
1995 – 1996
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| Keywords | Acute lung injury / Hypoxia / Pulmonary vascular permeability / Isolated lung / Polymorphonuclear leukocytes / Adgesion molecule / Myeloperoxidase |
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| Research Abstract |
Since pulmonary vascular permeability has been shown to increase under hyupoxic condition in rats, and since hypoxic exposure causes an accumulation of leukocytes in the pulmonary circulation, we hypothesized that PMN (polymorphonuclear leukocytes) contributes to hypoxia-induced acute lung injury. in this study, we investigated the effects of hypoxia and/or administration of PMN (polymorphonuclear leukocytes) on pulmonary microcirculation in isolated rat lungs. Pulmonary vascular permeability was assessed with the filtration coefficient (K) using gravimetric method. Hypoxia or PMN,when administered alon, did not affect the values of K,whereas, when combined, they proved to cause an increase in K.The myelo-peroxidase (MPO) levels of the hypoxia+PMN lungs were significantly higher than those of the noemoxia+PMN lungs. Exposure to hypoxia caused an increase in expression of Mac-1 (CD11b/CD18) on PMN,and treatment with anti-CD18 MoAb inhibited the increase in both K and MPO levels induced by hypoxia+PMN.These results indicate that PMN contribute to the lung injury induced by hypoxia, interacting with the endothelial cells of pulmonary vessels.
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