PROPOFOL AND AUTONOMIC REFLEX FUNCTION IN HUMANS

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 recordings of efferent sympathetic vasoconstrictor outflow (from the peroneal nerve) were monitored. Baroreceptor perturbations were produced by bolus intravenous injections of nitroprusside (100 mu g) followed 60 s later by phenylephrine (150 mu g) These stimuli were delivered to subjects while conscious and during propofol anesthesia (200 mu g kg(-1) min(-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 conditions and during a lower infusion rate of propofol (100 mu g kg(-1) min(-1)) combined with 70% nitrous oxide. Propofol infusions significantly lowered sympathetic nerve activity (SNA) and blood pressure (BP) and increased heart rate (HR). Cardiac baroreceptor sensitivity determined during nitroprusside was reduced 60% during propofol infusions and was only subtly improved during simultaneous N2O administration. In contrast, reflex sensitivity during phenylephrine was not changed from awake values during each of the three experimental conditions. Reflex regulation of SNA was nearly abolished during normocarbic conditions under propofol anesthesia but restored to conscious levels during hypercarbia and during N2O administration. These data indicate that propofol markedly attenuates reflex responses to hypotension, but that reflex sympathetic responses are better maintained in hypercarbic conditions and when lower doses of propofol are used in conjunction with N2O. In contrast, reflex responses to a hypertensive stimulus seem to be well preserved during propofol infusions regardless of the prevailing Pace, or the presence of N2O.