2002 Fiscal Year Final Research Report Summary
Developing the therapeutic methods for mitochondrial function, which may related to the neuronal recovery in penumbral region
| Project/Area Number |
12671470
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | OKAYAMA UNIVERSITY |
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Principal Investigator |
NAGANO Osamu OKAYAMA UNIVERSITY, University hospital, Assistant professor, 医学部附属病院, 助手 (30263586)
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| Co-Investigator(Kenkyū-buntansha) |
MORITA Kiyoshi OKAYAMA UNIVERSITY, Graduate School of Medicine and Dentistry, Professor, 大学院・医歯学総合研究科, 教授 (40108171)
TAKEDA Yoshimasa OKAYAMA UNIVERSITY, University hospital, Assistant professor, 医学部附属病院, 助手 (30294466)
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| Project Period (FY) |
2000 – 2002
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| Keywords | Mitochondria / Penumbra / NADH |
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| Research Abstract |
To elucidate the propagation of recurrent depolarization in the penumbra, the fluorescence of cortical NADH was observed in rats that had been subjected to focal ischemia. Ischemia was initiated by tightening the left CCA ligature and occluding the MCA by lifting the vessel 1 mm above the cortical surface with an 80-μm stainless-steel hook attached to a micromanipulator. A large cranial window was made on the left parietal-temporal bone to observe almost the entire left cortical hemisphere. The cortical surface was illuminated using a UV lamp (366nm), and images of NADH fluorescence were taken every 17 seconds using a CCD camera with a 460nm bandpass filter. During a three-hour period of ischemia, 220 recurrent depolarizations were observed in 45 animals as waves of high signal intensity that originated at the edge of the ischemic core and moved along the round margin of the ischemic core. Recurrent depolarizations were classified into two types : "spread-out type (86%)" in which recurrent depolarization spread out and did not increase the area of the ischemic core, and "expansion type (14%)" in which recurrent depolarization merged with the ischemic core and increased the area of the ischemic core. Histological examination revealed that neuronal injury occurred in the penumbral region, in which "spread-out type" of recurrent depolarization was observed, and that infarction occurred in the ischemic core, in which "expansion type" of recurrent depolarization was observed.
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