Propofol, but not etomidate, reduces desflurane-mediated sympathetic activation in humans

The administration of desflurane to humans can lead to substantial activation of the neurohumoral axis. Propofol can inhibit the sympathetic response to stress. This study compared the neurocirculatory effects of induction of anesthesia with propofol with those of etomidate on desflurane-mediated sympathetic activation.

After informed consent, awake baseline recordings of heart rate (HR), mean arterial blood pressure (MAP), and efferent sympathetic nerve activity (SNA, peroneal nerve) were obtained from healthy volunteers randomly assigned to receive either 2.5 mg x kg(-1) propofol (n=8) or 0.3 mg x kg(-1) etomidate (n=7). Two minutes after i.v. induction, desflurane 3.6% was added to the inspired gas, and increased in consecutive minutes to 7% and 10.9%. Ventilation via mask was continued for an additional seven minutes. Normocarbia was maintained while neurocirculatory parameters were continuously recorded.

There were no differences between groups at baseline. The administration of desflurane via mask after etomidate led to increases in HR, MAP and SNA. Propofol significantly reduced the MAP response and delayed and attenuated the sympatho-excitation.

Propofol induction reduced the sympathetic activation and hypertension associated with desflurane.