G. Bodelsson et al., Effects of propofol on substance P-induced relaxation in isolated human omental arteries and veins, EUR J ANAES, 17(12), 2000, pp. 720-728
To elucidate if an effect of propofol on endothelium-dependent relaxation c
ould contribute to propofol-induced vasodilation, smooth muscle relaxation
of isolated human omental artery and vein segments precontracted by endothe
lin-1 were measured. Substance P induced a concentration-dependent relaxati
on (mean +/- SEM) in both artery (63 +/- 8.4% of precontraction, n = 9) and
vein (60 +/- 11%, n = 7). The relaxation was enhanced by 10(-6) m propofol
(artery, 72 +/- 9.5%, n = 9; vein, 81 +/- 12%, n = 7) but not affected by
10(-7), 10(-5) and 10(-4) m propofol. In the presence of N-omega-nitro-l-ar
ginine methyl ester (nitric oxide synthase inhibitor), 10(-6) m propofol st
ill enhanced the substance P-induced relaxation in arteries but not veins,
whereas 10(-4) m propofol inhibited the relaxation in both arteries (rightw
ard shift of the concentration-response curve) and veins (28 +/- 7.5%, n =
8). In the presence of potassium chloride (to prevent hyperpolarization), t
he enhancement of substance P-induced relaxation by 10(-6) m propofol was a
bolished in both arteries and veins whereas 10(-5) and 10(-4) m propofol re
duced the relaxation in arteries (38 +/- 13% at 10(-5) m, n = 6; 30 +/- 11%
at 10(-4) m, n = 6) but not in veins. These results demonstrate that propo
fol, at lower, clinically relevant concentrations, promotes endothelium-dep
endent relaxation mediated via hyperpolarization in human omental arteries
and via both nitric oxide and hyperpolarization in human omental veins.