Jm. Hynson et al., THERMOREGULATORY VASOCONSTRICTION DURING PROPOFOL NITROUS-OXIDE ANESTHESIA IN HUMANS - THRESHOLD AND OXYHEMOGLOBIN SATURATION, Anesthesia and analgesia, 75(6), 1992, pp. 947-952
To determine the thermoregulatory effects of propofol and nitrous oxid
e, 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 wa
s induced with an intravenous bolus dose of propofol (2 mg/kg), follow
ed by an infusion of 180 mug.kg-1.min-1 for 15 min, and maintained wit
h 60% nitrous oxide and propofol (80-160 mug.kg-1.min-1). Central and
skin surface temperatures and Spo2 (using two different pulse oximeter
s) were measured continuously; plasma propofol concentrations and arte
rial Po2 were measured at 15-min intervals. Volunteers were cooled wit
h a circulating water blanket until definitive peripheral vasoconstric
tion was detected. The tympanic membrane temperature triggering vasoco
nstriction was considered the thermoregulatory threshold. Vasoconstric
tion developed on seven study days during propofol/nitrous oxide anest
hesia at a central temperature of 33.3 +/- 1.0-degrees-C (mean +/- SD)
and plasma propofol concentration of 3.9 +/- 1.1 mug/mL. The threshol
ds during anesthesia were significantly lower than those during the co
ntrol period (36.7 +/- 0.3-degrees-C), but the correlation between pla
sma propofol concentrations and vasoconstriction thresholds was poor.
On the remaining six study days, vasoconstriction did not develop desp
ite central temperatures ranging from 32.1 to 32.7-degrees-C. Correspo
nding propofol concentrations were 4.1-10.9 mug/mL. These data suggest
that anesthesia with propofol, in typical clinical concentrations, an
d 60% nitrous oxide substantially inhibits thermoregulatory vasoconstr
iction. Vasoconstriction increased Spo2 by approximately 2% without a
significant concomitant change in Po2. The observed increase in Spo2 p
robably reflects decreased transmission of arterial pulsations to veno
us blood in the finger.