The morphine-like agonists (morphine, meperidine, oxymorphone) have primary activity at the _mu_ receptors, with some activity possible at the delta receptor. The primary pharmacologic effects of these agents include: analgesia, antitussive activity, respiratory depression, sedation, emesis, physical dependence, and intestinal effects (constipation/defecation). Secondary pharmacologic effects include: _CNS:_ euphoria, sedation, and confusion. _Cardiovascular:_ bradycardia due to central vagal stimulation, alpha-adrenergic receptors may be depressed resulting in peripheral vasodilation, decreased peripheral resistance, and baroreceptor inhibition. Orthostatic hypotension and syncope may occur. _Urinary:_ Increased bladder sphincter tone can induce urinary retention. Morphine’s CNS effects are irregular and are species specific. Cats, horses, sheep, goats, cattle, and swine may exhibit stimulatory effects after morphine injection, while dogs, humans, and other primates exhibit CNS depression. Both dogs and cats are sensitive to the emetic effects of morphine, but significantly higher doses are required in cats before vomiting occurs. This effect is a result of a direct stimulation of the chemoreceptor trigger zone (CTZ). Other species (horses, ruminants, and swine) do not respond to the emetic effects of morphine. Like meperidine, morphine can affect the release of histamine from mast cells. Morphine is an effective centrally acting antitussive in dogs. Following morphine administration, hypothermia may be seen in dogs and rabbits, while hyperthermia may be seen in cattle, goats, horses, and cats. Morphine can cause miosis (pinpoint pupils) in humans, rabbits, and dogs. While morphine is considered a respiratory depressant, respirations are stimulated initially in dogs. Panting may ensue which may be a result of increased body temperature. Often however, body temperature may be reduced due to a resetting of the “body’s thermostat.” As CNS depre
coronary vasoconstriction with resultant increase in coronary vascular resistance, and a transient decrease in arterial pressure. Both bradycardias and tachycardias have been reported in dogs. While morphine has been used for years as a sedative/analgesic in the treatment of myocardial infarction and congestive heart failure in people, its effects on dogs make it a less than optimal choice in canine patients with clinical signs of cardiopulmonary failure. However, its use has been recommended by several clinicians in the initial treatment for cardiogenic edema. The effects of morphine on the gastrointestinal (GI) tract consist primarily of a decrease in motility and secretions. The dog, however, will immediately defecate following an injection of morphine, then exhibit the signs of decreased intestinal motility and, ultimately, constipation can result. Both biliary and gastric secretions are reduced following administration of morphine, but gastric secretion of HCl will later be compensated by increased (above normal) acid secretion. Initially, morphine can induce micturition, but with higher
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