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Effects of propofol on bronchoconstriction and bradycardia induced by vagal nerve stimulation

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Vagolysis has been considered as a mechanism by which propofol produces bronchodilation. However, it has also been suggested that propofol-induced bradycardia may result from increased vagal tone. In this study, we have determined whether propofol has vagolytic effects on both the airway and cardiovascular system. Methods: 

Mongrel dogs were anesthetized with pentobarbital. Bronchoconstriction was assessed by measuring changes in a bronchial cross-sectional area (BCA) using a bronchoscopic method. Heart rate (HR) and direct arterial blood pressure were also monitored. Vagal nerve stimulation (VNS) was performed for 60 s to produce both bronchoconstriction and bradycardia. To determine the effect of propofol on VNS-induced bronchoconstriction and bradycardia (n = 7), 0 (saline), 2.0 and 20 mg/kg propofol were administered intravenously at 20-min intervals with VNS commenced 5 min later. In addition, to determine if propofol-induced bradycardia is due to a vagomimetic action, two groups of six dogs were given 20 mg/kg propofol with or without 0.2 mg/kg atropine pre-treatment. HR was measured before and 5 min after propofol. Results: 

Propofol 20 mg/kg significantly inhibited VNS-induced bronchoconstriction. Although propofol per se significantly reduced HR (24%) and blood pressure (37%), the reduction in HR produced by VNS after 20 mg/kg propofol did not differ from that after saline or the lower dose of propofol (2 mg/kg). As atropine pre-treatment did not attenuate propofol-induced bradycardia, this response is unlikely to be simply due to vagomimetic actions. Conclusion: 

Propofol has vagolytic effects on the airway but does not worsen bradycardia produced by parasympathetic stimulation.

Keywords: bradycardia; bronchoconstriction and vagal nerve stimulation; propofol

Document Type: Research Article


Affiliations: Department of Anesthesiology, University of Hirosaki School of Medicine, Hirosaki, Japan

Publication date: 2003-10-01

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