Abstract
Eight dogs were premedicated with tramadol (1.0 mg/kg [0.45 mg/lb], IM) and the other eight with morphine (1.0 mg/kg [0.45 mg/lb], IM) 20 minutes prior to anesthetic induction. Anesthesia was induced with thiopental and maintained with halothane in oxygen delivered in a Bain system, with spontaneous respiration. Degree of sedation and occurrence of emesis were evaluated after preanesthetic medication. Dose of thiopental necessary to allow tracheal intubation was recorded and compared between the two groups. Arterial blood gas analyses were done before premedication and at 60 minutes of anesthesia. Tramadol produced no visible sedation and no vomit, while morphine induced a moderate degree of sedation in all dogs and vomit in 62% of them. Dose requirement of thiopental was significantly higher in the dogs premedicated with tramadol. Dogs premedicated with morphine had significantly higher PaCO 2 and lower pH at 60 minutes of anesthesia. Tramadol is not a reliable sedative and do not induce vomit in healthy dogs. The requirement of subsequent anesthetics may not be significantly reduced as compared with morphine. Dogs premedicated with tramadol are likely to maintain better intraoperative respiratory function than when premedicated with morphine. Clinically, tramadol may be useful for premedication of dogs where vomit is undesirable.
Highlights
Morphine is the opioid agonist to which other opioids are compared [21]
The purpose of this study was to compare the effects of tramadol and morphine on sedation, emesis, thiopental requirement for anesthetic induction and intraoperative respiratory function when used for premedication of dogs undergoing general anesthesia
Level of sedation was rated as none for dogs premedicated with tramadol and moderate for those premedicated with morphine
Summary
Morphine is the opioid agonist to which other opioids are compared [21]. It is used for preanesthetic medication in dogs [7]. The analgesic effects are mediated by a weak binding to μ-opioid receptors, and by inhibiting noradrenaline and serotonin uptake in the neurons of descending inhibitory pain pathways [4,17]. The (+)-enantiomer has high affinity for the m-opioid receptor and inhibits serotonin uptake, whereas the (-)-enantiomer is an inhibitor of norepinephrine uptake [17]. The metabolite, O-desmethyltramadol (M1), is active, with 200fold higher affinity for opioid receptors than the parent drug [18,19]. The hepatic biotransformation of tramadol is identical in humans and dogs
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