| Project/Area Number |
61570734
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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 | Chiba University |
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Principal Investigator |
HIRASAWA Hiroyuki Chiba University School of Medicine, 医学部, 助教授 (80114320)
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| Co-Investigator(Kenkyū-buntansha) |
OHTAKE Yoshio Chiba University School of Medicine, 医学部, 助手 (50194189)
SUGAI Takao Chiba University School of Medicine, 医学部, 講師 (10187627)
稲葉 英夫 千葉大学, 医学部・附属病院, 助手 (60159952)
橘川 征夫 千葉大学, 医学部附属病院, 講師 (20134398)
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| Project Period (FY) |
1986 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1988: ¥100,000 (Direct Cost: ¥100,000)
Fiscal Year 1987: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1986: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Acute Hepatic Failure / Reticuloendothelial (RES) Function / Opsonic Proteins / Fresh Frozen Plasma / 非特異的免疫賦活剤 / 急性肝不全ラット / ATP-MgCl_2 非特異的免疫賦活剤 / Kupffer細胞活性 / オプソニン活性 / 肝血流量 |
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| Research Abstract |
The present study was undertaken to investigate whether the reticuloendothelial (RES)phagocytic activity would be depressed in acute hepatic failure (AHF) and whether the enhancement of the depressed RES function would be beneficial in the treatment of AHF. In the experimental study AHF was induced with galactosamine in rats, and the RES phagocytic activity was measured with lipid emulsion method. Furthermore hepatic cellular mitochondrial function was investigated with arterial ketone body ratio (AKBR) and blood level of opsonic proteins such as C3 and fibronection was also investigated. The AHF rats showed the significant depressions in the RES phagocytic activity and AKBR, and depleted blood level of opsonic proteins. These rats were administered ATP-Mg to improve the impaired mitochondrial function and also given the non-specific immunomodulator, OK-432. With these treatments, the AHF rats showed the improvement in the RES phagocytic activity and AKBR, and the repletion of opsonic proteins. And most importantly the rats treated with ATP-Mg and/or OK-432 showed the improved survival rate compared to the AHR rats'without RES enhancement. Taking those results of the experimental study into consideration, the patients with AHF was given massive dose of fresh frozen plasma in order to improve the opsonic protein levels and OK-432 to enhance the RES function besides the conventional artificial liver support therapy with plasma exchange and hemoadsorption. The SHF patients showed the improvement in AKBR and opsonic protein levels and showed the better survival with these treatments. These results suggest that the depression in RES phabocytic activity can play one of the key roles in the pathogenesis of AHF and that the enhancement of the RES phagocytic activity could be beneficial in the treatment of the AHF.
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