1988 Fiscal Year Final Research Report Summary
A study of Etiology in experimental spinal cord injury
| Project/Area Number |
62480321
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Orthopaedic surgery
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| Research Institution | The University of Tokushima |
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Principal Investigator |
MURASE Masaaki School of Medicine, assistant, 医学部附属病院, 助手 (00182121)
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| Co-Investigator(Kenkyū-buntansha) |
MORIMOTO Kuniaki School of Medicine, assistant, 医学部附属病院, 助手 (80210186)
FUKUZAWA Kenji Faculty of Pharmaceutical Sciences, assistant professor, 薬学部, 助教授 (90035551)
OKA Motoo School of Medicine, Professor, 医学部, 教授 (60028298)
IKATA Takaaki School of Medicine, Professor, 医学部, 教授 (80108860)
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| Project Period (FY) |
1987 – 1988
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| Keywords | Spinal cord injury / Bitamin E / Thiobarbituric acid reactive substance(TBARS) / Thromboxane A_2 / prostaglandin I_2 / syringomyelia / 脊髄ー脊髄液関門 |
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| Research Abstract |
We studied lipid peroxidation and activation of arachidonate metabolism which trauma initiated in experimental rat spinal cord injury.
1. Lipid peroxidation Level of lipip peroxide was estimated as TBA-reactive substance(TBARS) in the spinal cord tissue. The level of TBARS increased promptly and was higher after 40-g compression than after 10-g or 20-g compression. The increased levels of TBARS were roughly proportional to the compression weights. The amount of TBARS produced was greater in vitamin E deficient and control group than in vitamin E-supplement group.
2. Activation of arachidonate metabolism We examined the changes of TXA_2 and PGI_2 levels in spinal cord compression injury. TXA_2 and PGI_2 are so labile that those were measured as TXB_2 and 6-keto-PGF_1 by redioimmunoassay respectively. The tissue TXB_2 level rapidly increased to a peak (133.6 X 13.8 pmol/g cord) 5 minutes after the injury with 20-g compression weight, while the 6-keto-PGF_1 level increased slightly. The magnitude of the increases of TXB_2 and the extent of post-traumatic vascular injury as determined by fluorescein uptake were both depended on the degree of spinal cord injury. These findings suggested that lipid peroxidation and activation of arachidonate metabolism played importand roles in spinal cord injury. The intramedullary morement of tracers (Fluorescein, Evans Blue, HRP, Lanthanum Chloride) following subarachnoid perfusion were examined morphologically in normal and Kaolin-induced syringomyelia rats. Reaction products of HRP were mainly in the extracellular space of the normal spinal cord. The pathologic spinal cord, however, allowed the passage of HRP into the parenchyma through the extracellular space of the marginal glia. Consequently, the extracellular space of the soinal cord constitutes a pathway for cerebrospinal fluid solutes.
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