Morphine exacerbates anaphylactic shock in mice by stimulating central opiate receptors.
Intravenous (i.v.) administration of 25 mg/kg morphine significantly increased mortality following induction of systemic anaphylaxis in mice. This effect was blocked by pretreatment with the opiate antagonist naltrexone but not by the selective peripherally acting antagonist naltrexone methyl bromide. Additionally, the effect of i.v. morphine was blocked by the opiate antagonist Win 44,441-3, but not by its inactive (+)-isomer Win 44,441-2. Furthermore, intracerebroventricular (i.c.v.) administration of 25 micrograms morphine increased anaphylactic mortality. This effect was blocked by i.v. naloxone. Finally, the effect of i.v. morphine, 25 mg/kg, on anaphylactic mortality was reversed by i.c.v. naloxone. Collectively, these findings demonstrate that morphine can exacerbate anaphylactic shock reactivity by stimulating specific CNS opiate receptors. The role of endogenous opiate mechanisms in the pathogenic sequence of circulatory shock is discussed.
D000707:Anaphylaxis / Q000139:chemically induced*; D000818:Animals; D001392:Azocines / Q000494:pharmacology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009020:Morphine / Q000494:pharmacology*; D009270:Naloxone / Q000031:analogs & derivatives* / Q000494:pharmacology; D009271:Naltrexone / Q000494:pharmacology*; D011957:Receptors, Opioid / Q000187:drug effects*
D001392:Azocines; D011957:Receptors, Opioid; D009270:Naloxone; D009271:Naltrexone; D009020:Morphine; C035969:quadazocine