DUAL RESPONSE OF CEREBROCORTICAL BLOOD-FLOW AND ARTERIAL BLOOD-PRESSURE TO TRANSIENT CO2 STIMULUS AFTER INHIBITION OF NITRIC-OXIDE SYNTHESIS IN RATS

Inhibition of nitric oxide synthase (NOS) by Nitro-L-arginine-methyl-e ster (L-NAME 15 mg and 70 mg/kg i.v.) in 16 male Wistar rats anaesthet ized with urethane, paralysed and artificially ventilated, increased s ignificantly local peripheral vascular resistance in the parietal cort ex (CVR) along with augmentation of the mean arterial blood pressure ( MAP) and no change of the local cerebrocortical blood flow (CBF) recor ded with a Laser-Doppler-Flowmeter. In II rats L-NAME reversed a press er effect of brief hypercapnia induced by 10% CO2/air mixture (PaCO2 8 4.1 +/- 5 mm Hg) into a depressor response, reduced CBF response propo rtionally to the reduction of MAP and did not influence CVR response t o CO2. In 5 rats L-NAME did not abolish the central presser effect of a CO2-stimulus and significantly augmented CO2-induced vasodilatatory response in the cortex (43.4 +/- 24% before L-NAME and 137.8 +/- 38.8% after L-NAME) by a larger reduction of CVR (-11 +/- 8% before L-NAME and -47.1 +/- 7.6% after L-NAME). It is concluded that NO does not med iate the vasodilatatory effect of brief hypercapnia in the cortex. NO appears critical for the central presser effect of CO2. In those rats in which the central presser effect of a CO2-stimulus was not abolishe d by an NOS blocker, an increased CBF and augmented decrease in CVR wa s observed during brief hypercapnia. Possible mechanisms of this dual responsiveness of cortical blood flow and arterial blood pressure to C O2, induced by inhibition of NOS, are discussed.