To determine the thermoregulatory effects of propofol and nitrous oxide, we measured the threshold for peripheral vasoconstriction in seven volunteers over a total of 13 study days. We also evaluated the effect of vasoconstriction on oxyhemoglobin saturation (Spo2). Anesthesia was induced with an intravenous bolus dose of propofol (2 mg/kg), followed by an infusion of 180 μg.kg−1.min−1 for 15 min, and maintained with 60% nitrous oxide and propofol (80–160 μg.kg−1.min−1). Central and skin surface temperatures and Spo2 (using two different pulse oximeters) were measured continuously; plasma propofol concentrations and arterial Po2 were measured at 15-min intervals. Volunteers were cooled with a circulating water blanket until definitive peripheral vasoconstriction was detected. The tympanic membrane temperature triggering vasoconstriction was considered the thermoregulatory threshold. Vasoconstriction developed on seven study days during propofol/nitrous oxide anesthesia at a central temperature of 33.3 ± 1.0°C (mean ± SD) and plasma propofol concentration of 3.9 ± 1.1 μg/mL. The thresholds during anesthesia were significantly lower than those during the control period (36.7 ± 0.3°C), but the correlation between plasma propofol concentrations and vasoconstriction thresholds was poor. On the remaining six study days, vasoconstriction did not develop despite central temperatures ranging from 32.1 to 32.7°C. Corresponding propofol concentrations were 4.1–10.9 μg/mL. These data suggest that anesthesia with propofol, in typical clinical concentrations, and 60% nitrous oxide substantially inhibits thermoregulatory vasoconstriction. Vasoconstriction increased Spo2by approximately 2% without a significant concomitant change in Po2. The observed increase in Spo2 probably reflects decreased transmission of arterial pulsations to venous blood in the finger.