The effects of continuous infusions of propofol on baroreceptor reflex
regulation of cardiac rate and peripheral sympathetic nerve activity
were evaluated in seven healthy, normotensive, young (19-26 yr), male
volunteers. Heart rate, radial artery pressure, and continuous recordi
ngs of efferent sympathetic vasoconstrictor outflow (from the peroneal
nerve) were monitored. Baroreceptor perturbations were produced by bo
lus intravenous injections of nitroprusside (100 mu g) followed 60 s l
ater by phenylephrine (150 mu g) These stimuli were delivered to subje
cts while conscious and during propofol anesthesia (200 mu g kg(-1) mi
n(-1)) at least 25 min after subjects were paralyzed (vecuronium), had
tracheas intubated, and were ventilated (30% O-2:70% N-2) to maintain
normocarbia. Additional data were collected during hypercarbic condit
ions and during a lower infusion rate of propofol (100 mu g kg(-1) min
(-1)) combined with 70% nitrous oxide. Propofol infusions significantl
y lowered sympathetic nerve activity (SNA) and blood pressure (BP) and
increased heart rate (HR). Cardiac baroreceptor sensitivity determine
d during nitroprusside was reduced 60% during propofol infusions and w
as only subtly improved during simultaneous N2O administration. In con
trast, reflex sensitivity during phenylephrine was not changed from aw
ake values during each of the three experimental conditions. Reflex re
gulation of SNA was nearly abolished during normocarbic conditions und
er propofol anesthesia but restored to conscious levels during hyperca
rbia and during N2O administration. These data indicate that propofol
markedly attenuates reflex responses to hypotension, but that reflex s
ympathetic responses are better maintained in hypercarbic conditions a
nd when lower doses of propofol are used in conjunction with N2O. In c
ontrast, reflex responses to a hypertensive stimulus seem to be well p
reserved during propofol infusions regardless of the prevailing Pace,
or the presence of N2O.