Desflurane increases heart rate independent of sympathetic activity in dogs

Desflurane has been shown to increase sympathetic activity and heart rate (HR) in a concentration-dependent manner. Nevertheless, desflurane, like all other volatile anaesthetics, increased HR in parallel to vagal inhibition in a previous study. Therefore, our hypothesis is that desflurane elicits tachycardia by vagal inhibition rather than by activation of the sympathetic nervous system.

Six dogs were studied awake and during desflurane anaesthesia (1 and 2 MAC) alone, after pretreatment with propranolol (2 mg kg(-1) followed by 1 mg kg(-1) h(-1)), or after pre-treatment with atropine (0.1 mg kg(-1) followed by 0.05 mg kg(-1) h(-1)). The effects on HR and HR variability were compared by an analysis of variance (P < 0.05). HR variability was analysed in the frequency domain as power in the high-(0.15-0.5 Hz, vagal activity) and low-frequency range (0.04-0.15 Hz, sympathetic and vagal activity).

HR increased during 2 MAC of desflurane from about 60 (awake) to 118 +/- 2 beats min(-1) (mean +/- SEM) in controls and to 106 +/- 3 beats min(-1) in dogs pre-treated with propranolol. In contrast, pretreatment with atropine increased HR from 64 +/- 2 to 147 +/- 5 beats min(-1) (awake) and HR decreased to 120 +/- 5 beats min(-1) after adding desflurane. High-frequency power correlated inversely with HR (r2 = 0.95/0.93) during desflurane alone and in the presence of beta-adrenoceptor blockade, with no significant difference between regression lines. There was no correlation between these variables during atropine/desflurane.

The increase in HR elicited by desflurane mainly results from vagal inhibition and not from sympathetic activation.