Dual response of cerebrocortical blood flow and arterial blood pressure to transient CO2 stimulus after inhibition of nitric oxide synthesis in rats
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Inhibition of nitric oxide synthase (NOS) by Nitro-L-arginine-methyl-ester in 16 male Wistar rats anaesthetized with urethane, paralysed and artificially ventilated, increased siginficantly local peripheral vascular resistance in the parietal cortex (CVR) along with augmentatoin of the mean arterial blood presure (MP) and no change of the local cerebrocortical blood flow (CBF) recorded with a Laser-Doppler-Flowmeter.In 11 rats L-NAME reversed a pressor effect of brief hypercapnia induced by 10% Co2/air mixture into depressor esponse,reduced CBF esponse proportionally to the reduction of MAP and did notinfluence CVR response to CO2. In 5 rats L-NAME did not abolish the central pressor effect of CO2-stimulus and significantly augmented CO2-induced vasodilatory response in the cortex by a larger reduction of CVR.It is concluded that NO does not mediate the vasodilatory effect of brief hypercapnia in the cortex.NO apears critical for the central pressor effect of CO2.In those rats in which the central pressor effect of a CO2-stimulus was not abolished by an NOS blocker, an increased CBF and augmented decrease in CVR was observed during brief hypercapnia.Possible mechanisms of this dual responsiveness of cortical blood flow and arterial blood pressure to CO2, induceds bu inhibition of NOS, are discussed.
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