›› 2011, Vol. 31 ›› Issue (2): 165-.doi: 10.3969/j.issn.1674-8115.2011.02.010

• Original article (Basic research) • Previous Articles     Next Articles

Vasodilation effect of propofol on isolated rat thoracic aorta rings

WEN Xiang-yu1,2, CUI Yong-yao3, JIANG Wei2, WANG Li2   

  1. 1.Department of Postgraduate, Soochow University, Suzhou 215006, China;2.Department of Anesthesiology, The Sixth People's Hospital, Shanghai Jiaotong University, Shanghai 200233, China;3.Department of Pharmacology, Basic Medical College, Shanghai Jiaotong University, Shanghai 200025, China
  • Online:2011-02-28 Published:2011-03-01
  • Supported by:

    National Natural Science Foundation of China, 30972842;Shanghai Natural Science Foundation, 09ZR1424000


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