THE EFFECTS OF CLONIDINE ON DESFLURANE-MEDIATED SYMPATHOEXCITATION INHUMANS

This study explored the effectiveness of oral clonidine premedication in attenuating sympathetic activation, tachycardia, and hypertension t riggered by desflurane. After institutional review board approval, inf ormed consent was obtained from 15 young, healthy male volunteers. Hea rt rate (HR, electrocardiogram), mean arterial pressure (MAP, radial a rtery catheter), and central venous pressure (CVP, jugular vein) were monitored. Recordings of sympathetic nerve activity (SNA) were obtaine d 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 hou r later, repeat recordings were obtained. Propofol (2.5 mg/kg) and vec uronium (0.15 mg/kg) were given intravenously. Ventilation via a mask (100% O-2) was used to maintain normocarbia. Two minutes after propofo l administration, the desflurane vaporizer was set at 3.6% (0.5 minimu m alveolar anesthetic concentration [MAC]) and increased at 1-min inte rvals 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 w ere obtained at 5.4%, during the first 5 min after advancing the vapor izer from 5.4% to 11% (''transition''), and at 11%. Resting HR, MAP, a nd 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 induc tion and transition periods. Steady-state effects of desflurane were s imilar between groups. The clonidine-treated subjects were more somnol ent and required a longer stay in the recovery area prior to home disc harge. Desflurane has the unique ability to increase SNA, leading to s ubstantial increases in HR and MAP. The present study demonstrates tha t clonidine is partially effective in reducing desflurane-mediated res ponses.