| Project/Area Number |
06670072
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
General physiology
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| Research Institution | National Cardiovascular Center Research Institute |
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Principal Investigator |
NAKAI Masatsugu National Cardiovascular Center Research Institute, LABORATORY HEAD, 循環動態機能部, 室長 (90150226)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1995: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1994: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Cerebral circulation / Cerebral blood flow / Cerebral energy metabolism / Parasympathetic nerve / Superior salivatory nucleus / Periaqueductal gray / Arterial barorecepror / 動脈圧反射 / 侵害刺激 / 副交感神経中枢 |
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| Research Abstract |
1.The aim of the present project was to find higher centers which govern the parasympathetic cerebrovasodilator center (the greater petrosal nerve cell group of the superior salivatory nucleus). As a first step, experiments were conducted on anesthetized, artificially ventilated, and cervically cordotomized rats, with special regard to the periaqueductal gray matter (PAG) as one of the higher centers.
2.Chemical stimulation of the PAG region with NMDA provoked a huge increase in cortical blood flow (CoBF ; microsphere flowmetry ; 100%, n=30), without significant changes in arterial blood pressure.Furthermore, we observed an only moderate enhancement (52%) of cortical metavolic rate for O_2. This finding indicates that the PAG-induced CoBF increase was provoked by certain mechanisms of non-metabolic origin to the extent of about one-half.
3.In view that the parasympathetic cerebrovasodilation will be independent of the cerebral oxidative metabolism, we consider that the non-metabolic component of the PAG-induced CoBF increase might be mediated by the parasympathetic center.
However, we found that the PAG-induced CoBF increase was pentolinium-resistant and scopolamine-sensitive. This pattern of responses to these pharmacological blockade was the exact reverse of what observed with the parasympathetic cerebrovasodilation.
We therfore conclude that the PAG has notheing to do with the cerebrovasodilator action of the parasympathetic center.
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