| Project/Area Number |
01570864
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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 |
麻酔学
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| Research Institution | Hiroshima University |
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Principal Investigator |
OHTANI Minako Hiroshima Univ. Univ., Hospital Associate Professor, 医学部附属病院, 助教授 (10033995)
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| Co-Investigator(Kenkyū-buntansha) |
KAJIHARA Hiroki Hiroshima Univ. Organization Office for College of Medical Tech. Professor, 医療技術短期大学部創設準備室, 教授 (20034184)
OKABAYASHI Kiyoshi Hiroshima Univ. Univ., Hospital Assistant Professor, 医学部附属病院, 講師 (50127627)
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| Project Period (FY) |
1989 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1991: ¥200,000 (Direct Cost: ¥200,000)
Fiscal Year 1990: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1989: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Shock phase in burns / Kupffer cells / Phagocytic activity / Endotoxin / White pulp of Spleen / Cell necrosis / 脾臓白脾髄 / リンパ濾胞 / 濾胞辺縁帯 / 貪食能 / 遊離ヘモグロビン / マクロファ-ジ |
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| Research Abstract |
The reticuloendothelial system(RES)is an essential component of the non-specific host defense system which clears circulating debris, such as aggregated protein, damaged cells and fibrin from the bloodstream, in addition to removing blood-borne bacteria.
We studied changes in plasma haemoglobin levels and morphology of Kupffer cells in rats following lethal thermal injury. The plasma haemoglobin levels rapidly increased to a maximum level 15 minutes after injury and then rapidly decreased with time. However, the values were still higher 5 hours after injury than those found before injury. Soon after burning the Kupffer cells phagocytized not only circulating cell debris including erythrocyte membranes and degenerate leucocytes but also large amounts of haemoglobin. This phagocytized haemoglobin is considered to inhibit the generation of bactericidal-free radicals and to depress Kupffer cell function. The number of Kupffer cells was markedlly decreased 5 hours after thermal injury, and probably relates to the persistent depletion of the reticuloendothilial system function which follows lethal thermal injury. In contrast to the decreased number of Kupffer cells, a small number of monocytic cells appeared in the sinusoidal spaces and adhered to the endothelial cells.
Our findings suggest that blood monocutes might migrate to the sinusoidal wall and transform into Kupffer cells. We also studied the effect of endotoxin on Kupffer cells in the rat liver following 30% thermal injury of body surface area. The Kupffer cells were markedly degenerate in the early stage.
Structural changes of the white pulp of the spleen were investigated in rats following thermal injury. Tingible bodies and tingible body macrophages were abundant in germinal center, follicular are and perifollicullar zone.
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