1996 Fiscal Year Final Research Report Summary
Study on the effects of nitric oxide on cerebral blood flow in developmental brain.
| Project/Area Number |
07457244
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Kobe University |
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Principal Investigator |
NAKAMURA Hajime Kobe University, School of Medicine, Professor, 医学部, 教授 (40030978)
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| Co-Investigator(Kenkyū-buntansha) |
TSUNEISHI Shuichi Kobe University, School of Medicine, Assistant, 医学部附属病院, 助手 (10271040)
YONETANI Masahiko Kobe University, School of Medicine, Assistant, 医学部, 助手 (60221678)
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| Project Period (FY) |
1995 – 1996
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| Keywords | Nitric oxide / Hypoxia / Cerebral blood flow / development / Striatum |
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| Research Abstract |
The present study was performed to investigate the role of nitric oxide (NO) in regulation of regional cerebral blood flow (CBF) during hypoxia and reoxygenation in developing rats striatum. The production of nitric oxide (NO) production in rat striatum was measured by using a NO-selective amperometric microsensor. We inserted the working electrode into the right striatum and monitored NO response continuously throughout the experiment. CBF in striatum was measured by laser Doppler flowmetry throughout the experimental period. Following stabilization, rats were subjected to 60-min hypoxia with 8% O2 and the subsequent 60-min reaxygenation with 21% O2. In 7-day-old rets, we observed a gradual increase in NO release by 116(]SY.+-。[)29 pA in the course of hypoxia and a secondary increase by 191(]SY.+-。[)31 pA during reoxygenation. In 14-day-old rats, the amount of an increase of NO released in response to hypoxia and that of another increase induced by reoxygenation were 849(]SY.+-。[)189
… More
and 847(]SY.+-。[)196 pA,respectively. They were singificantly greater thon those in 7-day-old rats. CBF decreased to 92(]SY.+-。[)3% of baseline during hypoxia and increased to124(]SY.+-。[)3% of vaseline during reoxygenation in 7-day-old rats, whereas CBF increased by both hypoxia and reoxygenation in 14-day-old rats to 125(]SY.+-。[)6% and 168(]SY.+-。[)6% of baseline, respectively. Pretreatment with L-NAME pretreatment with a NO synthase inhibitor, N-nitro-L-arginine methyl ester remarkably attenuated NO release during hypoxia and reoxygenation at both ages. Treatrment with L-NAME signifcantly attencated the hyperemic to hypoxia and/or reoxyg enation in both eges. also significantly attenuated the hyperemic responses to hypoxia and/or reoxygenation in both ages. Our present study demonstrates that the NO microelectrode can detect nanomolar levels of NO released in developing brain. Smaller NO release induced by hypoxia and reoxygenation in younger rats may indicate that immature brain has less abitity to aciivate NO synthase than more developed brain. Our results also indicated that the alteration of CBF during hypoxia and reoxygenation are associated with in vivo NO production. Less
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