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Öğe Gabapentin is a first line drug for the treatment of neuropathic pain in spinal cord injury(LIPPINCOTT WILLIAMS & WILKINS, 2004) Levendoglu, F; Ogun, CO; Ozerbil, O; Ogun, TC; Ugurlu, HStudy Design. Prospective, randomized, double blind, placebo-controlled, crossover clinical trial. Objectives. To determine the efficacy of gabapentin in the treatment of neuropathic pain related to spinal cord injury. Summary of Background Data. Neuropathic pain is initiated or caused by a primary lesion or dysfunction in the nervous system. Neuropathic pain associated with spinal cord injury is quite refractory, and current treatments are not effective. Gabapentin, an anticonvulsant, has become the first choice in the treatment of neuropathic pain. The place of gabapentin in the treatment of spinal cord injury-related neuropathic pain was questioned in only a few recent reports; however, they are retrospectively designed, nonstandardized, and uncontrolled studies, or involve a very small series of patients using less than optimum doses. Methods. A total of 18-week study period included a 4-week medication/ placebo titration period. This was followed by a 4-week stable dosing period when the patients continued to receive maximum tolerated doses, a 2-week washout period, then a crossover of 4 weeks of medication/ placebo titration, and another 4 weeks of stable dosing period. Twenty paraplegic patients (female/male: 7/13) with complete spinal cord injury at the thoracic and lumbar level, aged between 20 and 65 years, with neuropathic pain for more than 6 months were recruited for the study. Results. All patients completed the study. Gabapentin reduced the intensity as well as the frequency of pain, relieved all neuropathic pain descriptors except the itchy, sensitive, dull, and cold types, and improved the quality of life ( P < 0.05). Conclusions. Gabapentin can be added to the list of first-line medications for the treatment of chronic neuropathic pain in spinal cord injury patients. It is a promising new agent and offers advantages over currently available treatments.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]
