Alfentanil Modifies the Neurocirculatory Responses to Desflurane

Abstract

Activation 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.

Desflurane, compared to halothane, augments phenylephrine-induced contraction in isolated rat aorta smooth muscle

“…6 Alfentanil has been shown to effectively blunt the hemodynamic changes associated with rapid increases in inspired desflurane concentration, without reducing activation of the sympathetic nervous system. 8 Therefore, the hypertension associated with a rapid increase in desflurane level may not be mediated solely by increased sympathetic outflow. The interaction of desflurane with PE, which we have demonstrated, suggests that a local interaction between desflurane and endogenous catecholamines or increased catecholamine release from adventitial nerve endings may occur.…”

“…6 , 7 In addition, the hemodynamic changes can be blunted independently of the sympathetic outflow response to rapidly increased desflurane concentration. 8 The interaction of desflurane locally with the action of α-agonists on vascular smooth muscle is unknown. The effect of halothane on vascular ring vasomotion responses as well as its interaction with endothelium-dependent vasodilatation has been well characterised.…”

Desflurane - Revisited

“…Prior administration of alfentanil, fentanyl, sufentanil, clonidine, or β-adrenergic blocking drugs can minimize the sympathetic and/or CVS response. [3536] Desflurane provided more rapid control of hemodynamic response to surgical stimulation than isoflurane at high (3 l/min)[37] as well as low (1 l/min)[38] FGF rates.…”

Optimal dose of remifentanil for the prevention of hemodynamic responses during induction of anesthesia with desflurane

“…It is especially dangerous to patients with cardiovascular or cerebrovascular disease. Cardiovascular stimulation produced by desflurane can be attenuated by using opioids, β-blockers, and α 2-agonists [2][3][4][5]. However, the drug with a long duration of action may cause hypotension during the period without stimulation after endotracheal intubation.…”