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Effects of propofol on substance P-induced relaxation in isolated human omental arteries and veins

Bodelsson, Gunilla LU ; Sandstrom, K; Wallerstedt, S M; Hidestal, J; Tornebrandt, K and Bodelsson, Mikael LU (2000) In European Journal of Anaesthesiology 17(12). p.720-728
Abstract
To elucidate if an effect of propofol on endothelium-dependent relaxation could contribute to propofol-induced vasodilation, smooth muscle relaxation of isolated human omental artery and vein segments precontracted by endothelin-1 were measured. Substance P induced a concentration-dependent relaxation (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 Nomega-nitro-L-arginine methyl ester (nitric oxide synthase inhibitor), 10(-6) M propofol still enhanced the substance P-induced relaxation in arteries but not veins, whereas... (More)
To elucidate if an effect of propofol on endothelium-dependent relaxation could contribute to propofol-induced vasodilation, smooth muscle relaxation of isolated human omental artery and vein segments precontracted by endothelin-1 were measured. Substance P induced a concentration-dependent relaxation (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 Nomega-nitro-L-arginine methyl ester (nitric oxide synthase inhibitor), 10(-6) M propofol still enhanced the substance P-induced relaxation in arteries but not veins, whereas 10(-4) M propofol inhibited the relaxation in both arteries (rightward shift of the concentration-response curve) and veins (28+/-7.5%, n = 8). In the presence of potassium chloride (to prevent hyperpolarization), the enhancement of substance P-induced relaxation by 10(-6) M propofol was abolished in both arteries and veins whereas 10(-5) and 10(-4) M propofol reduced 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 propofol, at lower, clinically relevant concentrations, promotes endothelium-dependent relaxation mediated via hyperpolarization in human omental arteries and via both nitric oxide and hyperpolarization in human omental veins. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
anaesthetics, intravenous, propofol, tachykinins, substance P, arteries, omental, veins, endothelium, vascular.
in
European Journal of Anaesthesiology
volume
17
issue
12
pages
720 - 728
publisher
European Society of Anaesthesiology
external identifiers
  • pmid:11122309
  • scopus:0033635351
ISSN
1365-2346
DOI
10.1046/j.1365-2346.2000.00749.x
language
English
LU publication?
yes
id
2859934d-7396-4e0c-8b81-7f3ab4ca7d22 (old id 1116907)
date added to LUP
2008-07-02 12:58:04
date last changed
2017-01-01 05:14:05
@article{2859934d-7396-4e0c-8b81-7f3ab4ca7d22,
  abstract     = {To elucidate if an effect of propofol on endothelium-dependent relaxation could contribute to propofol-induced vasodilation, smooth muscle relaxation of isolated human omental artery and vein segments precontracted by endothelin-1 were measured. Substance P induced a concentration-dependent relaxation (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 Nomega-nitro-L-arginine methyl ester (nitric oxide synthase inhibitor), 10(-6) M propofol still enhanced the substance P-induced relaxation in arteries but not veins, whereas 10(-4) M propofol inhibited the relaxation in both arteries (rightward shift of the concentration-response curve) and veins (28+/-7.5%, n = 8). In the presence of potassium chloride (to prevent hyperpolarization), the enhancement of substance P-induced relaxation by 10(-6) M propofol was abolished in both arteries and veins whereas 10(-5) and 10(-4) M propofol reduced 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 propofol, at lower, clinically relevant concentrations, promotes endothelium-dependent relaxation mediated via hyperpolarization in human omental arteries and via both nitric oxide and hyperpolarization in human omental veins.},
  author       = {Bodelsson, Gunilla and Sandstrom, K and Wallerstedt, S M and Hidestal, J and Tornebrandt, K and Bodelsson, Mikael},
  issn         = {1365-2346},
  keyword      = {anaesthetics,intravenous,propofol,tachykinins,substance P,arteries,omental,veins,endothelium,vascular.},
  language     = {eng},
  number       = {12},
  pages        = {720--728},
  publisher    = {European Society of Anaesthesiology},
  series       = {European Journal of Anaesthesiology},
  title        = {Effects of propofol on substance P-induced relaxation in isolated human omental arteries and veins},
  url          = {http://dx.doi.org/10.1046/j.1365-2346.2000.00749.x},
  volume       = {17},
  year         = {2000},
}