NITROUS OXIDE AND NEURAL CONTROL OF THE CIRCULATION

Nitrous oxide causes pupillary dilation, diaphoresis, and increases in systemic vascular resistance, central blood volume, and forearm vascular resistance in volunteers during halothane anesthesia,^[457] suggesting that nitrous oxide activates the sympathetic nervous system. A subsequent study demonstrated that nitroux oxide does increase sympathetic nerve traffic measured using sympathetic microneurography in human volunteers,^[459] especially during the first 15 to 30 minutes of exposure to this anesthetic gas. Although baroreceptor reflex-mediated control of heart rate is impaired during administration of nitrous oxide, regulation of sympathetic outflow to peripheral blood vessels is preserved.^[458] This finding suggests nitrous oxide does not alter sympathetic vasoconstrictor-induced maintenance of arterial pressure and may be partially responsible for the relative stability of hemodynamics during nitrous oxide anesthesia.