BACKGROUND AND OBJECTIVE: 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. METHODS: 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). RESULTS: 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. CONCLUSIONS: The increase in HR elicited by desflurane mainly results from vagal inhibition and not from sympathetic activation.
BACKGROUND AND OBJECTIVE: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. METHODS: 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). RESULTS: 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. CONCLUSIONS: The increase in HR elicited by desflurane mainly results from vagal inhibition and not from sympathetic activation.