Abstract:

Objective To investigate the effect of propofol on isolated rat thoracic aorta rings, and explore the possible mechanism. Methods Vascular rings were randomly divided into endothelium-intact group and endothelium-denuded group, and each group was then divided into 5 subgroups: 10^-6 mol/L norepinephrine (NA) group (n=6), 10^-6 mol/L NA+propofol group (n=6), 10^-6 mol/L NA+0.18% intralipid group (n=6), 10^-6 mol/L NA+10^-4 mol/L propofol group(n=6), 10^-5 mol/L glibenclamide+10^-6 mol/L NA+propofol group (n=6), 10^-4 mol/L L-NAME +10^-6 mol/L NA+propofol group (n=6) (this subgroup was not included in endothelial-denuded group). On the basis of maximal vasoconstriction evoked by NA （10^-6 mol/L）, propofol was added in progressively increasing cumulative concentrations（10^-6, 5×10^-6, 10^-5, 5×10^-5 and 10^-4  mol/L）at a 15 minute interval, and the effect of propofol on artery was observed as vascular tone changed. Results Propofol induced vasorelaxation at a concentration-dependent manner, and the effect was most significant in endothelium-intact group, with the vasodilation extent of （11.28±1.51）%,（25.23±4.03）%,（44.08±4.49）%,（66.28±4.83）% and (74.59±4.78）%，respectively, which were significantly different from those in endothelium-denuded group with same management （P<0.01）. Propofol-induced vasodilation was inhibited by L-NAME (10^-4 mol/L), a nitric oxide synthase inhibitor (P<0.01）, and was also suppressed by glibenclamide, a specific inhibitor of KATP channels in endothelium-intact aorta. In addition, the vasodilation induced by 10^-6 mol/L and 5×10^-6 mol/L propofol was reversed by glibenclamide. Conclusion Propofol causes vasodilation of isolated thoracic aorta rings in rats in endothelium-dependent and concentration-dependent manners，and nitric oxide and KATP channels can mediate drug-induced vasodilation.

Key words: propofol, thoracic aorta, vasodilation, nitric oxide, KATP channels