Recently, it is generally accepted that endogenous opioid peptides play an important role in regulation of the immune response. Naloxone, an opiate-receptor antagonist has been used extensively in studies in which in which antagonism of morphine
or
other agents was considered a criterion for implicating endogenous opiates and/or their receptor in the action of such agents. The present study was undertaken in an effort to investigate the vivo effect of naloxone on humoral and cellular immune
response in mice, particularly the effect on active systemic anaphylaxis9ASA). The immune responses investigated were delayed-type hypersensitivity (DTH0 reactions to sheep red blood cells(SRBC), contact hypersensitivity to
dinitrofluorobenzene(DNFB)
and antibody by egg albumin(OVA). For the ASA experiment, mice were sensitized by intraperitoneal injection of 500μg OVA. 1.0mg alumn and 2×10E9 bordetella pertussis in 0.5ml PBS and were challenged by i.v. injection of 0.25 ml PBS containing
500μg
OVA 18 days after sensitization. A single intraperitoneal administration of naloxone910mg/kg) 3 hr prior to SRBC or DNFB challenge enhanced significantly DTH reaction and contact sensitivity, but did not affect antibody response to SRBC and PVP.
Interestingly, naloxone, given 1mg/kg or 10mg/kg 10min, 20min, 90min or 180min proior to shock induction with OVA, inhibitedd intensity of ASA and improved survival in experimental anaphylaxis in mice. The administration of higher dose of
naloxone(10m,g) led to more pronounced protective effect. Hematocrit value was decreased in naljoxone-pretreated mice relative to mice injected with saline. Taken together, this study may strongly suggested that endogenous opioid peptide may
contribute
to shock pathophysiology and naloxone has a protective effect from fatal anaphylactic shock. This study also indicate that naloxone may be important adjuncts in the prevention or treatment of active systemic anaphylactic shock.
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