Nitrous oxide augments sympathetic outflow: direct evidence from human peroneal nerve recordings.

Direct evidence for postganglionic sympathetic nerve activation to blood vessels supplying skeletal muscle was sought by recording from the peroneal nerve of 13 volunteers with a 5-mu tipped tungsten needle. Eight subjects breathed through an anesthesia face mask connected to a semiclosed anesthesia circuit for two consecutive 10-min periods while 25% and 40% nitrous oxide (N2O) was administered sequentially. Five subjects served as controls and breathed equivalent concentrations of nitrogen. Blood pressure and central venous pressure were recorded from radial artery and jugular vein catheters. Forearm blood flow was measured by venous occlusion plethysmography. Peroneal nerve recordings were amplified 100,000-fold and integrated for analysis of burst frequency. N2O did not significantly alter respiratory rate, end-tidal CO2 (mass spectrometry), and diastolic or central venous pressures but did produce small but significant increases in heart rate and systolic pressure compared to time-control (P less than 0.05). In contrast, N2O was associated with progressive, large increases in muscle sympathetic nerve activity (peak % delta = 69 +/- 22 burst/min [X +/- SEM]) and forearm vascular resistance (30 +/- 4%) and a nonsignificant increase in plasma norepinephrine levels. Thus, brief exposure to 25% and 40% N2O produces striking increases in sympathetic outflow to skeletal muscle in humans.