Nitric oxide does not act as a mediator coupling cerebral blood flow to neural activity following somatosensory stimuli in rats

Q. Wang, T. Kjaer, M. B. Jorgensen, O. B. Paulson, N. A. Lassen, N. H. Diemer, H. C. Lou*

*Corresponding author af dette arbejde

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    Abstrakt

    The possible role of nitric oxide (NO) on vibrissa-stimulated increase of regional cerebral cerebral blood flow (rCBF) and cerebral metabolic rate of glucose (rCMR(glu)) was investigated in conscious Wistar rats by using an inhibitor of NO synthase, N(G)-nitro-L-arginine (NOLAG) at a concentration of 30 mg/kg. In vivo autoradiography distribution with 14C-iodoantipyrine and 14C-deoxyglucose in two separate series showed CBF of 174% of control and CMR(glu) of 196% of control in the primary sensory cortex opposite the stimulated side in saline treated control animals. Similar increases were found in NOLAG-treated animals. Furthermore, NOLAG did not change either basal CMR(glu) or CMRO2. The findings suggest, that NO is not involved in coupling flow to the increased metabolism accompanying physiological sensory stimuli.

    OriginalsprogEngelsk
    Sider (fra-til)33-36
    Antal sider4
    TidsskriftNeurological Research
    Vol/bind15
    Udgave nummer1
    DOI
    StatusUdgivet - 1 jan. 1993

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    Udforsk hvilke forskningsemner 'Nitric oxide does not act as a mediator coupling cerebral blood flow to neural activity following somatosensory stimuli in rats' indeholder.

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