Propofol, bradycardia and the Bezold-Jarisch reflex in rabbits

Propofol may cause profound bradycardia and asystole, which are mediated in directly via cardiac innervation but could involve direct: effects on the s ino-atrial (SA) node and the conducting system of the heart. To test the hy pothesis that propofol may also activate Bezold-Jarisch reflexes to cause b radycardia, 5-hydroxytryptamine (5-HT), veratridine and propofol were injec ted into the left ventricle of the heart in both intact and vagotomized rab bits. 5-HT and veratridine produced an acute, rapid, dose-dependent decreas e in mean heart rate (Delta HR) and a decrease in mean arterial pressure (D elta MAP) together with transient but severe depression and abolition of re nal sympathetic nerve activity (RSNA). Bilateral vagotomy greatly attenuate d these responses; for example, at the highest dose of 5-HT (8 mu g 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, reduc tions in Delta HR and Delta MAP produced by propofol were statistically sig nificant 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 res ponses. These results indicate that the cause of acute bradycardia after ad ministration of propofol does not involve the Bezold-Jarisch reflex.