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Department of Anesthesiology and Intensive Care, Celal Bayar University, Manisa, Turkey
Address correspondence and reprint requests to Ismet Topcu, MD, Guzelyurt Mah. Ingolstadt Cad., Anadolu Konutlari No:11, 45030 Manisa, Turkey. Address e-mail to topcuismet{at}yahoo.com.
In this study, we investigated the effects of tramadol and fentanyl on gastrointestinal transit (GIT) during acute systemic inflammation in an experimental model of cecal ligation and perforation (CLP). One-hundred-twenty male Swiss-Albino rats were divided randomly into 6 groups: Group I = sham-operated + saline; Group II = sham-operated + fentanyl; Group III = sham-operated + tramadol; Group IV = CLP + saline; Group V = CLP + fentanyl; Group VI = CLP + tramadol. Suspension of charcoal was administered as an intragastric meal to measure the GIT. GIT% (mean ± sd) were 46.1% ± 9.8%, 43.2% ± 9.8%, 45.9% ± 10.2%, 33.2% ± 9.2%, 24.9% ± 4.1%, and 31.8% ± 8.4% in Groups I, II, III, IV, V, and VI, respectively. GIT% was significantly less in Group V than in Groups I, II, III, and IV (P < 0.05). The Group VI mean value was significantly lower than those of Groups I, II, and III (P < 0.05) but not different from those of Groups IV and V (P > 0.05). The antitransit effect of fentanyl was shown to have increased in the experimental sepsis model, but no decrease in GIT was obtained with tramadol. This was thought to be the result of an associated endogenic opioid system activation and receptor upregulation in sepsis.
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