• D Ma, M K Chakrabarti, and J G Whitwam.
• Department of Anaesthetics and Intensive Care, Imperial College School of Medicine, Hammersmith Hospital, London, UK.
• Br J Anaesth. 1999 Mar 1; 82 (3): 412-7.

AbstractPropofol may cause profound bradycardia and asystole, which are mediated indirectly via cardiac innervation but could involve direct effects on the sino-atrial (SA) node and the conducting system of the heart. To test the hypothesis that propofol may also activate Bezold-Jarisch reflexes to cause bradycardia, 5-hydroxytryptamine (5-HT), veratridine and propofol were injected into the left ventricle of the heart in both intact and vagotomized rabbits. 5-HT and veratridine produced an acute, rapid, dose-dependent decrease in mean heart rate (delta HR) and a decrease in mean arterial pressure (delta MAP) together with transient but severe depression and abolition of renal sympathetic nerve activity (RSNA). Bilateral vagotomy greatly attenuated these responses; for example, at the highest dose of 5-HT (8 micrograms kg-1), delta HR, delta MAP and duration of abolition of RSNA were reduced by 57% (P < 0.001), 53% (P < 0.05) and 79% (P < 0.05), respectively. In contrast, reductions in delta HR and delta MAP produced by propofol were statistically significant only at very high doses (8 mg kg-1). Propofol depressed but did not abolish RSNA, and bilateral vagotomy had no effect on any of these responses. These results indicate that the cause of acute bradycardia after administration of propofol does not involve the Bezold-Jarisch reflex.

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