| Project/Area Number |
08671713
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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 | AKITA UNIVERSITY (1997)
University of Tsukuba (1996) |
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Principal Investigator |
NISHIKAWA Toshiaki Akita University School of Medicine, Professor, 医学部, 教授 (50156048)
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| Co-Investigator(Kenkyū-buntansha) |
HASHIMOTO Kenji Yoshitomi Pharmaceutical Co., Ltd., 1st Research Institute of Drug Development,, 創薬第一研究所主任, 研究職
TAKAHASHI Hiroshi Tsuchiura Kyodo Hospital, Department of Anesthesia and Critical Care Medicine, C, 麻酔科長, 研究職
SATO Shigehito University of Tsukuba, Institute of Clinical Medicine, Associate Professor, 臨床医学系, 助教授 (30143176)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1997: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1996: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | Focal cerebral ischemia / Neuronal damage / sigma-receptor / Pentazocine / 一過性局所脳虚血 / シグマ受容体リガンド / 脳保護作用 |
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| Research Abstract |
1996
Rats underwent focal cerebral ischemia using the filament occlusion technique for 2h, followed by 22h of reperfusion. Rats received saline or 1mol/kg per hour 4-phenyl-1- (4-phenylbutyl) piperidine (PPBP), the potent sigma-receptor ligand, by continuous intravenous infusion starting 1 h after the initiation of ischemia and continuing through 22h of reperfusion. Triphenyltetrazolium-determined infarction volume of ipsilateral striatum (PPBP,19(]SY.+-。[)4 mm<@D13@>D1, mean(]SY.+-。[)SEM) was smaller in rats treated with PPBP than in control (44(]SY.+-。[)4 mm<@D13@>D1) rats. However, because of variability within groups, the effect of PPBP to reduce total ipsilateral cortex infarction volume (PPBP,80(]SY.+-。[)28 mm<@D13@>D1 ; saline, 136(]SY.+-。[)27mm<@D13@>D1) did not reach statistical significance.
1997
Rats underwent focal cerebral ischemia using the filament occlusion technique for 2h, followed by 22h of reperfusion. Rats received (+) or (-)-pentazocine at a dose of 2mg/kg/h by continuous intravenous infusion from 1 h of ischemia to 22h of reperfusion. Triphenyltetrazolium-determined infarction volume of ipsilateral striatum ([+]-pentazocine, 19(]SY.+-。[)4mm<@D13@>D1 ; [-]-pentazocine, 44(]SY.+-。[)5mm<@D13@>D1) and cerebral cortex ([+]-pentazocine, 26(]SY.+-。[)12mm<@D13@>D1 ; [-]-pentazocine, 134(]SY.+-。[)29mm<@D13@>D1) was smaller in rats treated with (+) compared with (-)-pentazocine. Infarction volume in rats treated with (-)-pentazocine was also very similar to the infarction volume in saline-treated control rats from our previous study. These data indicate that sigma<@D21@>D2-receptors may play an important role in the mechanism of injury both in cortex and striatum after 2h of transient focal ischemia in rats.
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