›› 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

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