• A E Yonker-Sell, M Muzi, W G Hope, and T J Ebert.
• Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, USA.
• Anesth. Analg. 1996 Jan 1;82(1):162-6.

AbstractActivation of the sympathetic nervous system occurs in response to desflurane, causing tachycardia and hypertension. Fentanyl partially blunts the hemodynamic effects of desflurane but fails to attenuate the sympathetic response. This study determined the clinical effectiveness and dose response of alfentanil on the neurocirculatory responses to desflurane. Twenty-five healthy, male volunteers were randomized into one of three groups to receive either placebo (n = 9), 10 micrograms/kg intravenous (IV) bolus alfentanil (n = 9), or 20 micrograms/kg IV bolus alfentanil (n = 7) in conjunction with anesthetic induction by propofol, 2.5 mg/kg. Mean arterial pressure (MAP, radial artery), heart rate (HR), and efferent muscle sympathetic nerve activity (SNA, peroneal nerve) were recorded. After conscious baseline measurements, anesthesia was induced by propofol and alfentanil/placebo. One minute later, the desflurane vaporizer was activated at 11%. Neurocirculatory measurements were recorded for 11 min. There were no differences between the groups at conscious baseline. Induction of anesthesia was associated with significantly decreased MAP in the placebo and the 10 micrograms/kg alfentanil groups and increased HR in all groups with little change in SNA. In placebo subjects, desflurane administration increased HR and MAP above baseline. In both alfentanil groups, during desflurane administration HR and MAP never increased significantly above baseline. However, SNA was significantly increased in both groups. Alfentanil effectively blunts the hemodynamic changes but not the sympathetic responses associated with rapid increases in the inspired concentration of desflurane.

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