NITRIC OXIDE SYNTHASE INHIBITOR SUPPRESS THE VASOCONSTRIC-TION DUE TO SEVOFLURANE IN CEREBRAL PIAL ARTERIES LARGER THAN 100μm IN DIAMETER IN CATS

Abstract

Background Nitric oxide (NO) plays an important role in the reactivity of cerebral circulation to various stimuli. It is still unclear whether NO mediates the effect of sevoflurane on cerebral circulation. We therefore examined this question by measuring the diameter of pial arteries with or without exposure to NO synthase inhibitor, N ω-nitro-L -arginine methyl ester (L-NAME). Methods The cranial window technique was employed in experiments using seven cats that received fentanyl and midazolam under mechanical ventilation. Diameters of cerebral pial arteries were observed through the cranial windows using an incident-light fluorescence microscope and video-recorded with a silicon-intensified target tube video camera system. Changes in arterial diameter were measured with an image analyzer after the experiments were finished. The diameters of pial arteries were measured under four conditions follow- ing the protocol below : 1) intravenous anesthesia ; 2) intravenous plus sevoflurane anesthe- sia; then after L-NAME infusion, 3) intravenous anesthesia ; and 4) intravenous plus sevoflurane anesthesia. Changes in vessel diameter were analyzed. Results The arteries larger than 100μm were significantly constricted (p<0.05) under sevoflurane inhalation ; in contrast, after the administration of L-NAME, the arteries were not significantly affected by sevoflurane inhalation. Conclusion L-NAME inhibited the vasoconstriction due to sevoflurane inhalation in cere- bral pial arteries larger than 100μm. In the cerebral pial arteries larger than 100μm in diameter, NO synthesis was shown to be involved in vasoconstriction due to sevoflurane inhalation.