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Öğe The effects of adding diphenhydramine hydrochloride to lidocaine in intravenous regional anaesthesia(VSP BV, 2003) Reisli, R; Celik, J; Tuncer, S; Apilliogullari, S; Duman, A; Yosunkaya, A; Okesli, SThis study aimed to evaluate whether diphenhydramine hydrochloride (DPH) could be used to reduce the dose of lidocaine for intravenous regional anaesthesia (IVRA). Sixty patients undergoing upper limb operations were divided into three groups (20 each). All patients received IVRA as follows: group 1 received 3 mg/kg lidocaine, group 2 received 40 mg DPH and 1.5 mg/kg lidocaine, and group 3 received 1.5 mg/kg lidocaine diluted to 40 ml with 0.9% saline solution. The onset of sensory block was tested by a pinprick. The duration of anaesthesia time was also recorded. Intraoperative pain was assessed using a five point pain score system. Side effects during surgery and after release of the tourniquet were recorded. Only 4 patients in group 3 had sufficient analgesia. Therefore, the patients in group 3 were excluded from the study. Data from 40 patients (group I and 2) were analysed. The onset time of sensory block was significantly shorter in group I than group 2 (2.4 +/- 1.54 min and 6.85 +/- 1.46 min, respectively). The tourniquet pain time was also significantly longer in group I than in group 2 (57.15 +/- 10.90 min and 42.65 +/- 9.67 min, respectively). One patient from each group experienced tinnitus for 30-60 s, and 4 patients in group 2 had minimal sedation after tourniquet release. According to our results, DPH is a safe and useful adjunct to IVRA in minor procedures of short duration. Decreasing the dose of lidocaine also decreases the risk of local anaesthetic toxicity in the event of accidental release of tourniquet pressure.Öğe The in vitro effects of remifentanil and fentanyl on isolated human right atria and saphenous veins(W B SAUNDERS CO, 2003) Duman, A; Sahin, AS; Atalik, KE; Ogun, C; Ulusoy, HB; Durgut, K; Okesli, SObjective: To determine the myocardial and vascular effects of remifentanil and fentanyl in human atria and saphenous veins. Design: In vitro, prospective with repeated measures. Setting: University research laboratory. Interventions: The direct effects of remifentanil and fentanyl on the electrical stimulation-induced contraction of nonfailing human atrium and saphenous veins contracted with 5-hydroxytryptamine were studied. Measurements and Main Results: In human atrial trabeculae, cumulative (10(-9)-10(-5) mol/L) added remifentanil had in 0 effect on contractile force, compared with untreated muscles (p > 0.05). The force of contraction was significantly less than control values with concentrations of fentanyl ranging from 10(-8) to 10(-5) mol/L (p < 0.05). At the highest concentration (10(-5) mol/L), the inhibition by fentanyl of the electrical stimulation-induced contraction was 40.6% +/- 6.32%. In human saphenous vein strips preconstricted with 5-hydroxytryptamine, remifentanil (10(-8)-10(-5) mol/L) and fentanyl (10(-8)-10(-5) mol/L) produced "concentration-dependent" relaxation when compared with the control contraction value (p < 0.05). The IC50 was similar with remifentanil and fentanyl and the E-max of fentanyl was significantly higher than remifentanil (p < 0.05). The venodilatory effects of remifentanil and fentanyl were similar on veins with or without endothelium (p > 0.05). Conclusions: Remifentanil has no direct effect on the contraction of myocardium. Fentanyl inhibits the electrical stimulation-induced contraction in human right atrial muscles in vitro. Remifentanil and fentanyl produce "concentration-dependent" relaxation in human saphenous vein strips independent from the endothelium. (C) 2003 Elsevier Inc. All rights reserved.Öğe 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, UObjective: 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.Öğe Remifentanil has different effects on thoracic aorta strips in different species, in vitro(BLACKWELL MUNKSGAARD, 2004) Duman, A; Ogun, CO; Sahin, AS; Atalik, KE; Erol, A; Okesli, S[Abstract not Available]
