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Sympathetic Excitation during Nitrous Oxide—Halothane Anesthesia in the Cat

The effect of 70 per cent nitrous oxide on preganglionic sympathetic activity was studied by recording the compound action potential from the splanchnic nerve in the cat. Substitution of nitrous oxide for an equal concentration of nitrogen in the inspired mixture during steady-state halothane–nitrogen–oxygen anesthesia caused significant increases in splanchnic-nerve discharge and mean arterial pressure and a moderate increase in heart rate. When the carotid sinus and aortic baroreceptor nerves were sectioned, these responses were further accentuated and were accompanied by a 71 per cent incidence of cardiac arrhythmias. With continued halothane anesthesia, decerebration by transection of the brainstem at the midcollicular level completely suppressed the responses to nitrous oxide. Following the removal of halothane in decerebrate preparations, nitrous oxide acted as a depressant, producing marked decreases in heart rate in animals with intact baroreceptors and significant decreases in splanchnic-nerve activity in debuffered animals. These results indicate that the increase in sympathetic activity produced by nitrous oxide is neurally mediated and dependent on actions at suprapontine levels, the loci of which are undetermined. The study further suggests that the direct effect of nitrous oxide is depressant to vasomotor neurons at the brainstem or spinal level.