ROLE OF NITRIC-OXIDE IN THE ELEVATION OF CEREBRAL BLOOD-FLOW INDUCED BY ACETYLCHOLINE AND ANOXIA IN THE TURTLE

Nitric oxide (NO)-dependent regulation of brain blood flow has hithert o not been studied in reptiles. By observing the brain surface (telenc ephalon) of the freshwater turtle (Trachemys scripta) with epiillumina tion microscopy, we show that topical application of acetylcholine (AC h) induces an increase in CBF velocity that can be completely blocked by the NO synthase inhibitor N-G-nitro-L-arginine methyl ester (L-NAME ). The effect of L-NAME was reversed by L-arginine. Also, sodium nitro prusside (SNP), which decomposes to liberate NO, caused an increase in CBF velocity. By contrast, L-NAME could not block the increase in blo od flow velocity caused by anoxia. Interestingly, superfusing the brai n with ACh or SNP during anoxia had no effect on the blood flow veloci ty. The results suggest that NO is an endogenous vasodilator in the tu rtle brain, mediating the effects of ACh during normoxia. By contrast, anoxia does not rely on NO as a vasodilator.