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    The Effects of Caudal Bupivakaine and Bupivakaine +sufentanil on Postoperative Analgesia in Peadiatric Patients [çocuklarda Kaudal Bupivakain Ve Bupivakain +sufentan?l?in Postoperatif Analjezik Etkile?i]
    (2003) Tuncer, Sema; Yosunkaya, Alper; Reisli, Ruhiye; Tavlan, Aybars; Köstekci, H.; Otelcioğlu, Ş.
    Caudal block is a widely used method for postoperatif analgesia after lower abdominal, rectal and urogenital surgery in children. The aim of this study was to determine whether the addition of sufentanil to bupivacaine caudally prolongs the duration of analgesia and side effects compared with bupivacaine alone. Aged 3-10, fifty two boys were allocated randomly to two groups at the end of surgery. Children in group I received 0.125% bupivacaine 1 ml kg-1, group II received 0.5 ?g kg-1 sufentanil + 0.125% bupivacaine caudally. Postoperative pain was assessed according to Modified Pediatric Objective Pain Scale (MPOPS) 2, 4, 6, 8, 16 and 24h after operation. Time for first administration of analgesic, total number of analgesic doses required and side effects were recorded. Demeanor assessment was made according to tree-point scale (0= cheerful/calm, 1=restless, 2= tense/tearful) by ward nurse. No significant differences were found between two groups for the pain scores. There was no significant difference in the requirement for additional doses of analgesia. More Patients who had received caudal sufentanil with bupivacaine were cheerful and calm compared with those in bupivacaine group. The addition of sufentanil to bupivacaine for caudal block does not affect the analgesia duration but provides a quality analgesia in children.
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    Sufentanil ve Remifentanilin İzole Perfüze Rat Böbreği Üzerine Etkileri
    (2004) Barışkaner, H.; Tuncer, Sema; Otelcioğlu, Ş.; Doğan, N.; Yosunkaya, A.; Kılıç, M.
    In this in vitro study on isolated perfused rat kidney, the effects of indomethacin, NG-nitro-L arginin methyl ester (L-NAME), propranolol, naloxone, glibenclamide and tetraethylammonium (TEA) on the responses induced by fentanyl, sufentaniyl and remifentanil were investigated. In isolated perfused rat kidney, under a constant flow of 8-10 ml/min, mean basal perfusion pressure and the responses of used inhibitors or antagonists were recorded on a polygraph. Fentanyl (10-9-10-6 M), sufentanil (10 -9-10-6 M) and remifentanil (10-9-10 -6 M) caused a dose-dependent decrease in perfusion pressure raised by submaximum concentration of phenylephrine. Fentanyl induced relaxations were inhibited by glibenclamide (10-5 M, n = 5) and TEA (10-3 M, n = 5) (p < 0.05) but not indomethacin (10-5 M, n = 5), L-NAME (10-4 M, n = 5), propranolol (10-6 M, n = 5) and naloxone (10-6 M, n = 5) (p > 0.05). Both sufentanil- and remifentalin-induced relaxations were not inhibited by indomethacin (10 -5 M, n = 5), L-NAME (10-4 M, n = 5), propranolol (10 -6 M, n = 5), naloxone (10-6 M, n = 5) (p > 0.05) and glibenclamide (10-5 M, n = 5) but TEA (10-3 M, n = 5) was effective (p < 0.05). These results suggest that in isolated perfused rat kidney, K+ channels may play a role in fentanyl-, sufentanil- and remifentanil-induced relaxation by opening ATP sensitive-potassium channels and calcium-activated potassium channels.