TY - JOUR
T1 - Desflurane increases heart rate independent of sympathetic activity in dogs
AU - Picker, O.
AU - Schwarte, L. A.
AU - Schindler, A. W.
AU - Scheeren, T. W.L.
PY - 2003/12
Y1 - 2003/12
N2 - 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 β-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.
AB - 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 β-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.
KW - Anaesthetics, Inhalation
KW - Parasympathetic Nervous System
KW - Sympathetic Nervous System
UR - http://www.scopus.com/inward/record.url?scp=0344629199&partnerID=8YFLogxK
U2 - https://doi.org/10.1017/S0265021503001522
DO - https://doi.org/10.1017/S0265021503001522
M3 - Article
C2 - 14690095
SN - 0265-0215
VL - 20
SP - 945
EP - 951
JO - European Journal of Anaesthesiology
JF - European Journal of Anaesthesiology
IS - 12
ER -