| Project/Area Number |
10470311
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Akita University |
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Principal Investigator |
NAKAE Hajime Akita University, School of medicine, Research Associate, 医学部, 助手 (10254781)
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| Co-Investigator(Kenkyū-buntansha) |
INABA Hideo Kanazawa University, School of medicine, Professor, 医学部, 教授 (60159952)
TANAKA Hiroyuki Akita University, School of medicine, Associate Professor, 医学部, 助教授 (90266297)
町井 正人 秋田大学, 医学部, 助手 (50209467)
鈴木 一郎 秋田大学, 医学部, 助手 (80187707)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥5,900,000 (Direct Cost: ¥5,900,000)
Fiscal Year 2000: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1999: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1998: ¥4,500,000 (Direct Cost: ¥4,500,000)
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| Keywords | heme oxygenase / endotoxin / cytokines / procaltitonin / sepsis / burn / nitric oxide / エンドトキシン / 急性肺障害 / 潅流肺 |
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| Research Abstract |
Heme oxygenase (HO-1) is a stress reactive protein induced by heavy metals, endotoxin, heat shock, inflammatory cytokines, hormones, etc. as well as substrates. HO-1 plays an important role in heme and heme protein metabolism. Carbon monoxide produced from heme by this protein, like nitric monoxide, regulates the cyclic GMP concentration through guanyl cyclase to control vascular tonus. Controlling vascular tonus is necessary to maintain oxygen transport and microcirculation in tissues. HO-1 also functions as an anti-oxidant enzyme and is reported to inhibit cell damages due to oxidant. In addition, there is a report of decreased mortality after endotoxin was given with the expression of HO-1 mRNA induced.
The current study immunohitologically examined lungs and livers removed from burn rats. HO-1 mRNA is reported to histologically localize in the alveolar wall, bronchial wall, and alveolar macrophages in the liver. The current study revealed the expression of HO-1 in lung and liver perivascular cells in burn rats. The study also revealed the expression of a little amount of HO-1 in hepatic parenchymal cells. We may have played a leading role in this area because of no previous reports with burn animals. An additional study is being conducted with a group of animals given a competitive inhibitor of HO-1, zink protoporphyrin, to inhibit the expression of HO-1, and with a sepsis model created.
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