Proanaphylactic action of morphine is mediated through a central cholinergic mechanism.
Intracerebroventricular (i.c.v.) or intravenous (i.v.) administration of morphine (10 micrograms or 25 mg/kg, respectively) increased the mortality rate in experimental anaphylaxis in mice. This effect was blocked by the opiate antagonist naltrexone administered systemically (5 mg/kg) or i.c.v. (10 micrograms). Moreover, the effect of morphine was blocked by i.c.v. administration of the muscarine antagonist methyl atropine (10 micrograms). The systemic administration of 5 mg/kg methyl atropine was ineffective in blocking the action of morphine. The results suggest that the proanaphylactic effect of morphine involves activation of cholinergic mechanisms in the central nervous system.
D000707:Anaphylaxis / Q000503:physiopathology*; D000818:Animals; D001286:Atropine Derivatives / Q000494:pharmacology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009020:Morphine / Q000037:antagonists & inhibitors / Q000633:toxicity*; D009271:Naltrexone / Q000494:pharmacology; D010275:Parasympathetic Nervous System / Q000187:drug effects*
D001286:Atropine Derivatives; D009271:Naltrexone; D009020:Morphine; C006649:methylatropine