Differential effect of propofol on sympathetic neurotransmission in isolated human omental arteries and veins

1 The present study was undertaken to elucidate the effect of propofol on sympathetic neurotransmission in isolated human omental vessels. 2 Segments of both arteries and veins were exposed to 0, 10(-7), 10(-6), 10(-5) or 10(-4) M propofol? and studied in vitro to determine effects on: (i) isometric tension after electrical field stimulation (EFS) or after exogenous administration of noradrenaline (NA); (ii) EFS-stimulated release of [H-3]-NA from vessel segments preincubated with [H-3]-NA; (iii) uptake of [H-3]-NA. 3 Propofol at 10(-6) M enhanced EFS-induced contraction in artery segments, 10(-7) and 10(-5) M had no effect, and 10(-4) M propofol depressed EFS-induced contraction in both artery and vein segments. 4 Propofol did not affect the response to exogenous NA in artery and vein segments. 5 EFS-stimulated release of [H-3]-NA was depressed by 10(-5) and 10(-4) M propofol in artery segments, and by 10(-4) M in vein segments. 6 Uptake of [H-3]-NA was depressed by 10(-6)-10(-4) M propofol in artery but not in vein segments. 7 The results suggest that sympathetic neurotransmission is enhanced at clinical concentrations (10(-6) M) of propofol in human omental arteries, but not veins. This may be due to an increased availability of NA in the neuromuscular junction resulting from a reduced presynaptic reuptake. Propofol at probably supraclinical concentrations (10(-5)-10(-4) M) impairs the sympathetic neurotransmission in both human omental arteries and veins, probably due to an inhibitory effect on the NA release from the sympathetic nerves.