THE EFFECTS OF CLONIDINE ON DESFLURANE-MEDIATED SYMPATHOEXCITATION IN HUMANS

This study explored the effectiveness of oral clonidine premedication in attenuating sympathetic activation, tachycardia, and hypertension triggered by desflurane. After institutional review board approval, informed consent was obtained from 15 young, healthy male volunteers. Heart rate (HR, electrocardiogram), mean arterial pressure (MAP, radial artery catheter), and central venous pressure (CVP, jugular vein) were monitored. Recordings of sympathetic nerve activity (SNA) were obtained from the peroneal nerve via percutaneously placed tungsten needles. After baseline recordings, subjects were randomized to receive either a placebo (n = 10) or 0.3 mg of clonidine (n = 9) per os (PO). One hour later, repeat recordings were obtained. Propofol (2.5 mg/kg) and vecuronium (0.15 mg/kg) were given intravenously. Ventilation via a mask (100% O-2) was used to maintain normocarbia. Two minutes after propofol administration, the desflurane vaporizer was set at 3.6% (0.5 minimum alveolar anesthetic concentration [MAC]) and increased at 1-min intervals to 7.2% and 11% (1.0 and 1.5 MAC). After 10 min, the trachea was intubated and 20 min later steady-state neurocirculatory recordings were obtained at 5.4%, during the first 5 min after advancing the vaporizer from 5.4% to 11% (''transition''), and at 11%. Resting HR, MAP, and SNA were similar between the two groups. PO clonidine reduced SNA, CVP, and MAP but did not change HR. In both groups propofol decreased SNA and MAP, and increased HR. The administration of desflurane via a mask resulted in significant increases in SNA, HR, and MAP. Clonidine reduced the HR and MAP responses by approximately 30%-40% during induction and transition periods. Steady-state effects of desflurane were similar between groups. The clonidine-treated subjects were more somnolent and required a longer stay in the recovery area prior to home discharge. Desflurane has the unique ability to increase SNA, leading to substantial increases in HR and MAP. The present study demonstrates that clonidine is partially effective in reducing desflurane-mediated responses.