These studies will address how volatile anesthetics influence cerebral blood flow regulation. The first hypothesis is that differences in the hyperemic effects of various volatile anesthetics in specific brain regions are due to their different effects on regional neuronal activity which is coupled to the microvascular dilatation. They will determine the concentration-dependent and region-specific effects of three volatile anesthetics (halothane, isoflurane, and sevoflurane) on cerebrocortical microvascular perfusion and intraparenchymal microvessel diameter. They will determine if the relative degree of microvascular dilatation is dependent on the presence of spontaneous neuronal activity. The second hypothesis is that neuronal-derived NO plays an essential role in volatile anesthetic-induced microvascular dilation and hyperemia and that the anesthetic agent- and region-specific differences in these responses are in part neuronal NO-mediated. They will determine if neuronal and/or endothelial-derived NO modulate the differential, concentration-dependent responses of the cerebral microcirculation. The third hypothesis is that volatile anesthetic-induced vasodilatation is modulated by the anesthetic depression of spontaneous neuronal activity via enhancement of GABAergic effects and decreased production of NO. They will determine if regional and agent-specific differences in microvascular vasodilation in response to volatile anesthetics are due to the effects of these agents on the GABA and NO neuronal systems.
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