CLINICAL PHARMACOLOGY
Clinical trials have proven hydrocodone bitartrate to be an effective antitussive agent which is pharmacologically 2 to 8 times as potent as codeine. At equi-effective doses, its sedative action is greater than codeine. The precise mechanism of action of hydrocodone and other opiates is not known, however, hydrocodone is believed to act by directly depressing the cough center. In excessive doses hydrocodone, like other opium derivatives, will depress respiration. The effects of hydrocodone in therapeutic doses on the cardiovascular system is insignificant. The constipation effects of hydrocodone are much weaker than that of morphine and no stronger than that of codeine. Hydrocodone can produce miosis, euphoria, physical and psychological dependence. At therapeutic antitussive doses, it does exert analgesic effects. Following a 10 mg oral dose of hydrocodone administered to five adult male human subjects, the mean peak concentration was 23.6 ± 5.2 ng/mL. Maximum serum levels were achieved at 1.3 ± 0.3 hours and the half-life was determined to be 3.8 ± 0.3 hours. Hydrocodone exhibits a complex pattern of metabolism including O-demethylation, N-demethylation and 6-keto reduction to the corresponding 6-(alpha)- and 6-(beta)-hydroxymetabolites.
Chlorpheniramine maleate is a competitive H1-receptor histamine blocking drug, thereby counteracting the effects of histamine release associated with allergic manifestations of upper respiratory tract inflammatory disorders. H1-blocking drugs inhibit the actions of histamine on smooth muscle, capillary permeability, and can both stimulate and depress the central nervous system. Phenylephrine hydrochloride effects its vasoconstrictor activity by releasing noradrenaline from sympathetic nerve endings, and from direct stimulation of (alpha)-adrenoreceptors in blood vessels. Acetaminophen is an antipyretic and peripherally acting analgesic. Caffeine is a central nervous system stimulant.
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