Ulcetra Mechanism of Action

Pharmacology: Pharmacodynamics: Tramadol is a centrally acting synthetic opioid analgesic. Although its mode of action is not completely understood, from animal test, at least two complementary mechanism appear applicable: binding of parent and M1 metabolite to μ-opioid receptors and weak inhibition of norepinephrine and serotonin reuptake.
Opioid activity is due to both low affinity binding of the parent compound and higher affinity binding of the O-demethylated metabolite M1 to μ-opioid receptors. In animal models, M1 up is to 6 times more potent than Tramadol in producing analgesia and 200 times more potent in μ-opioid binding. Tramadol-induced analgesia is only partially antagonized by the opiate antagonist naloxone in several animal tests. The relative contribution of both Tramadol and M1 to human analgesia is dependent upon the plasma concentrations of each compound.
Tramadol has been shown to inhibit reuptake of norepinephrine and serotonin in-vitro, like some other opioid analgesics. These mechanisms may contribute independently to the overall analgesic profile of Tramadol.
Apart from analgesia, Tramadol administration may produce a constellation of symptoms (including dizziness, somnolence, nausea, constipation, sweating, and pruritus) similar to that of other opioids.
Paracetamol: Paracetamol is a non-opiate, non-salicylate analgesic.
Food Effects: When Ulcetra is administered with food, the time to peak plasma concentration was delayed for approximately 35 minutes for Tramadol and almost one hour for Paracetamol. However, peak plasma concentration, and the extents of absorption, of Tramadol and acetaminophen were not affected. The clinical significance of this difference is unknown.