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1994 Fiscal Year Final Research Report Summary

Mechanism for the Development of Irreversible Damages in Cerebral Ischemia.

Research Project

Project/Area Number 05404032
Research Category

Grant-in-Aid for General Scientific Research (A)

Allocation TypeSingle-year Grants
Research Field Neurology
Research InstitutionOsaka University

Principal Investigator

YANAGIHARA Takehiko  Osaka Univ., Dept.of Neurology, Professor, 医学部, 教授 (70243201)

Co-Investigator(Kenkyū-buntansha) UEDA Hirokazu  Osaka University Hospital, Dep.t of Neurology, Clinical Fellow, 医学部・付属病院, 医員
NAKAMURA Masaichi  Osaka Univ., Dept.of Neurology, Assistant Professor, 医学部, 助手 (50243225)
MATSUMOTO Masayasu  Osaka Univ., Dept.of Neurology, Assistant Professor, 医学部, 助手 (20192346)
Project Period (FY) 1993 – 1994
KeywordsCerebral Ischemia / Magnetic Resonance Imaging / Diffusion / Immunohistochemistry / Energy Metabolism / Microtubule-Associated Proteins / Selective Vulnerability / Cytotoic Edema
Research Abstract

To elucidate the pathophysiological mechanism for ischemic irreversible damage, we analyzed the sequential changes of biochemical and physiological parameters by use of HPLC,near infra-red spectro-photometry and magnetic resonance imaging, and compared them with the immunohistochemical changes in the gerbil model of cerebral ischemia.
1. We established the method for the simultaneous assessment of changes in regional levels of energy metabolites and immunohistochemical changes in brain tissues of 10 to 50 microgram dry weight. The decrease of regional ATP level seemed prerequisite for the development of immunohistochemical damages.
2. The diffusion-weighted magnetic resonance imaging showed prompt decrease of diffusion coefficient of tissue water, indicating ion pump failure as the results of energy failure caused cytoskeletal and cell damage.
3. The results by near-infrared spectroscopy indicated complete reduction of cytochrome oxidase seemed preceded for the decrease of ATP.
4. The comparison of vulnerability between tubulin and MAPIA indicated damages of tubulin seemed more closely related to irreversible damage than those of MAPIA in ischemia.
5. The regional decrease in N-acetyl aspartate levels was detected in the area of delayd neuronal death, indicating the sensitive marker for the neuronal loss and irreversible damages in the brain.
6. In hypoxia/reoxygenation model using cultured astrocytes, similar derangement of energy states and induction of stress proteins were observed as in the gerbil model of cerebral ischemia.
7. In hindbrain regions, selective vulnerability to the ischemia existed as in the case of forebrain ischemia. From these results, irreversible damages in cerebral ischemia could be the result of complete reduction of cytochrome oxidase, ATP depletion, ion pump failure, and degradation of cytoskeletal proteins.

  • Research Products

    (12 results)

All Other

All Publications (12 results)

  • [Publications] H.Tomimoto and T.Yanagihara: "Golgi electron microscopic study of the cerebral cortex after transient cerebral ischemia and reperfusion in the gerbil." Neuroscience. 63. 957-967 (1994)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] T. Yanagihara: "Controversies in vascular dementia." Hypertens.Res.17(Suppl.I). S103-S107 (1994)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] H.Ueda,et al: "N-acetyl aspartate levels in delayed neuronal death in the hippocampus of the gerbil brain." J.Neurochem.64(Suppl.). S13- (1995)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] R.Hata,et al: "An ischemic opening of the blood-brain barrier may deteriorate brain stem auditory evoked potentials following transient hindbrain ischemia in gerbils." Acta Neurochir.60(suppl.). 197-199 (1994)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Y.Maeda,et al: "Hypoxia/reoxygenation-mediated induction of astrocyte interleukin 6:a paracrine mechanism potentially enhancing neuron survival." J.Exp.Med.180. 2297-2308 (1994)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] K.Hashikawa,et al: "Split dose iodine-123-IMP SPECT: sequential quantitative regional cerebral blood flow change with pharmacological intervenntion." J.Nucl.Med.35. 1226-1233 (1994)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] H.Tomimoto and T.Yanagihara: "Golgi electron microscopic study of the cerebral cortex after transient cerebral ischemia and reperfusion in the gerbil." Neuroscience. 63. 957-967 (1994)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] T.Yanagihara: "Controversies in vascular dementia." Hypertens.Res.17 (Suppl.I). S103-S107 (1994)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Ueda, H.Matsumoto, M., Nakano, M,Li, JY,Yoshida, Y., Yanagihara T.: "N-acetyl aspartate levels in delayd neuronal death in the hippocampus of the gerbil brain." J.Neurochem.64 (Suppl.). S13 (1995)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Hata, R., Matsumoto, M., Yamamoto, K., Ohtsuki, T., Ogawa, S., Handa, N., Kubo, T., Matsunaga, T., Nishimura, T., Kamada, T.: "An ischemic opening of the blood-brain barrier may deteriorate brain stem auditory evoked potentials following transient hindbrain ischemia in gerbils." Acta Neurochir.60 (Suppl.). 197-199 (1994)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Maeda, Y., Matsumoto, M., Hori, O., Kuwabara, K., Ogawa, S., Yan, S.-D., Ohtsuki, T., Kinoshita, T., Kamada, T., Stern, D.: "Hypoxia/reoxygenation-mediated induction of astrocyte interleukin 6 : a paracrine mechanism potentially enhancing neuron survival." J.Exp.Med.180. 2297-2308 (1994)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Hashikawa, K., Matsumoto, M., Moriwaki, H., Oku, N., Okazaki, Y., Uehara, T., Hand, N., Kusuoka, H., Kamada, T., Nishimura, T.: "Split dose iodine-123-IMP SPECT : sequential quantitative regional cerebral blood flow change with pharmacological intervention." J.Nucl.Med.35. 1226-1233 (1994)

    • Description
      「研究成果報告書概要(欧文)」より

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Published: 1996-04-15  

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