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Ebert Thomas J. MD PhD; Muzi, Michael MD
Anesthesia & Analgesia: February 1994
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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 μg) followed 60 s later by phenylephrine (150 μg). These stimuli were delivered to subjects while conscious and during propofol anesthesia (200 μg-kg-1min-1) at least 25 min after subjects were paralyzed (vecuronium), had tracheas intubated, and were ventilated (30% O2:70% N2) to maintain normocarbia. Additional data were collected during hypercarbic conditions and during a lower infusion rate of propofol (100 μg.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 Paco2 or the presence of N2O.

This work was supported in part by a National Institutes of Health training grant no. GM 08377 and ICI-Stuart Pharmaceuticals.

© 1994 International Anesthesia Research Society