1993 Fiscal Year Final Research Report Summary
Studies on the Endotoxin Shock
| Project/Area Number |
03670309
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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 |
Legal medicine
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| Research Institution | University of Occupational and Environmental Health |
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Principal Investigator |
TANAKA Noriyuki UOEH・Forensic Medicine, Professor, 医学部, 教授 (60126597)
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| Co-Investigator(Kenkyū-buntansha) |
KITA Toshiro UOEH・Forensic Medicine, Associate Professor, 医学部, 助教授 (00131912)
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| Project Period (FY) |
1991 – 1993
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| Keywords | Endotoxin Shock / Tumor Necrosis Factor / Leukotriene / Lipopolysaccharide / Immunocytochemical Localization / Liver / Kidney / Heart / Lung |
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| Research Abstract |
Abundant inflammatory cells such as leukocytes and macrophages accumulated and adhered to the endothelial surface of the vascular vessels after administration of bacterial lipopolysaccharide(LPS). There is also marked endothelial cell damage including intracytoplasmic edema, increased numbers of autophagic vacuoles and dilatation of the intercellular junction in LPS-treated samples. The degeneration of parenchymal cells such as hepatic necrosis, renal proximal tubular cell necrosis and edematous muscle cells of the myocardium also observed in LPS-treated sample. The presence of immunocytochemical products of leukotriene(LT) and tumor necrosis factor(TNF) was examined using in LPS-treated samples. Immunoreactions of LT seen in the lysosomes of inflammatory cells attached to the endothelial cell surface may indicate the onset of endothelial cell damage. Positive immunoreactions of TNF on the endothelial cell surface indicate that TNF may enhance the adhesion of leukocytes to endothelium. In addition to these reactios sites, lysosomes of the degeneration of parenchymal cells such as hepatic necrosis, renal proximal tubular cell necrosis and edematous muscle cells of the myocardium were immunoreactive for TNF or LT.These degeneration of parenchymal cells is primarily caused by endogenous TNF or LT rather than by ischemia.
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Research Products
(6 results)
