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    Cooling and response to hydrogen peroxide in human saphenous vein: role of the endothelium
    (WILEY, 2005) Sahin, AS; Atalik, KE; Sahin, TK; Dogan, N
    In the present work we studied the responses of human saphenous vein to H2O2 and effects of moderate cooling on these responses with analysis of the role of endothelium. H2O2 (10(-7)-10(-2) m) induced concentration-dependent contraction in the intact human saphenous vein strips at both temperatures. At 28 degrees C, the maximal contraction induced by H2O2 was significantly lower than that at 37 degrees C. Compared with intact strips, the sensitivity and the maximal contraction to H2O2 were significantly enhanced in endothelium-denuded strips at 37 and 28 degrees C. However, pD(2) values and maximal contractions were not significantly different in endothelium-denuded strips at different temperatures. Pretreatment with N-G-nitro-L-arginine methyl ester (L-NAME) increased significantly the maximal contraction and sensitivity to H2O2 at 37 and 28 degrees C. The contractions increased by L-NAME were restored by the pre-incubation Of L-arginine (10(-3) m) at every temperature studied. The contractile responses of intact human saphenous veins to H2O2 were reduced significantly by 10(-5) m indomethacin at both temperatures. Our results suggest that H2O2-induced contraction of human saphenous vein are mediated by its direct effect on the smooth muscle and by the generation of products of the cyclooxygenase pathway from the endothelium. Signalling pathways of these contractile effects are the same at 3 7 and 28 degrees C. Under normal temperature conditions, the contraction to H2O2 is possibly modulated by endothelial nitric oxide. Cooling reduces the contraction to H2O2 by increasing release of nitric oxide.
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    The mechanisms of the direct vascular effects of fentanyl on isolated human saphenous veins in vitro
    (W B SAUNDERS CO-ELSEVIER INC, 2005) Sahin, AE; Duman, A; Atalik, EK; Ogun, CO; Sahin, TK; Erol, A; Ozergin, U
    Objective: The purpose of this study was to determine the mechanism of the direct effects of fentanyl on human veins in vitro. Design: In vitro, prospective with repeated measures. Setting: University research laboratory. Interventions: Dose-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), N omega-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 Results: Preincubation 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). Conclusions: The 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. (c) 2005 Elsevier Inc. All rights reserved.