• Ayşe Saide Sahin, Ateş Duman, Esra Kismet Atalik, Cemile Oztin Ogün, Tahir Kemal Sahin, Atilla Erol, and Ufuk Ozergin.
• Department of Pharmacology, Selcuk University, Akyokuş 42080, Konya, Turkey. aysesaide@hotmail.com
• J. Cardiothorac. Vasc. Anesth. 2005 Apr 1; 19 (2): 197-200.

ObjectiveThe purpose of this study was to determine the mechanism of the direct effects of fentanyl on human veins in vitro.DesignIn vitro, prospective with repeated measures.SettingUniversity research laboratory.InterventionsDose-response curves were obtained for cumulative doses of fentanyl (10(-9)-10(-5) mol/L) on saphenous vein strips precontracted with (10(-6) mol/L) 5-hydroxytryptamine incubated with either naloxone (10(-4) mol/L), Nomega-nitroL-arginine-methyl ester (L-NAME) (10(-4) mol/L), indomethacin (10(-5) mol/L), glibenclamide (10(-4) mol/L), tetraethylammonium (10(-4) mol/L), or ouabain (10(-5) mol/L). Vein strips were also exposed to a Ca++-free solution and 0.1 mmol/L of ethylene glycol-bis-(b-aminoethylether) N,N'-tetraacetic acid; 5-hydroxytryptamine (10(-6) mol/L) was added to the bath before cumulative Ca++ (10(-4)-10(-2) mol/L). The same procedure was repeated in the presence of fentanyl (10(-6) , 3 x 10(-6) , or 10(-5) mol/L) (p < 0.05 = significant).Measurements And Main ResultsPreincubation of vein strips with naloxone, L-NAME, or indomethacin did not influence the relaxant responses to fentanyl (p > 0.05). Tetraethylammonium, glibenclamide, and ouabain reduced the relaxation response to fentanyl (p < 0.05). A stepwise increase in tension was recorded with cumulative doses of Ca++ (p < 0.05).ConclusionsThe present results show that fentanyl causes vasodilatation via both endothelium- and opioid receptor-independent mechanisms in the human saphenous vein. The relaxant effects of fentanyl are probably via activation of K+ channel and Na+K+-adenosine trisphosphatase and inhibition of Ca++ channel.

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