| Project/Area Number |
15591634
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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 | Yamaguchi University |
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Principal Investigator |
FUKUDA Shirou Yamaguchi Univ., Hospital, Research Associate, 医学部附属病院, 助手 (70322245)
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| Co-Investigator(Kenkyū-buntansha) |
SAKABE Takefumi Yamaguchi Univ., School of Medicine, Professor, 医学部, 教授 (40035225)
MATSUMOTO Mishiya Yamaguchi Univ., School of Medicine, Associate Professor, 医学部, 助教授 (60243664)
ISHIDA Kazuyoshi Yamaguchi Univ., School of Medicine, Research Associate, 医学部, 助手 (80314813)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2004: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2003: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | ischemic tolerance / opioid receptors / neuronal injury / gerbil / forebrain ischemia / hippicampus / hematoxylin-eosin staining / naloxone / 虚血耐性様現象 / モルヒネ / 脳虚血 |
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| Research Abstract |
In this study, we examined the role of opioid receptors in ischemic-tolerance-like phenomenon by short period of forebrain ischemia. In male gerbils used bilateral common carotid afrter-occlusion model. Animals were divided into six groups : 5 min ischemia and 7 days reperfusion (Isch group), 2 min ischemia and 3 days reperfusion followed by 5 min ischemia and 7 days reperfusion (PC group), naloxone 3 mg/kg iv. followed by the sam condition as PC group (NX1 group), naloxone 0.03 mg/kg iv. followed by the same condition of PC group (NX2 group), and control group. After reperfusion after 5 min ischemia, all gerbils were perfused with formaldehyde, and the brain samples were evaluated for neuronal damage in the hippocampus with HE-staining. In control group, the CA1-2 region of hippocampus showed no damage. In Isch group, they were severely damaged revealing vacuolation and pyknosis of neurons. However, the neuronal injury in hippocampus was significantly better in PC group compared to the other groups. In NX1 and NX2 groups, the CA1-2 regions were again worse than control group, and the neurons in hippocampus were also worse in M group. These findings suggest that the involvement of opioid receptors, possibly other than ?-receptors in the phenomenon of ischemic tolerance.
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