naloxone and Immunologic-Deficiency-Syndromes

Topics: Adult; Antibody Formation; Cells, Cultured; Cytotoxicity, Immunologic; Disease Susceptibility; Endorphins; Heroin Dependence; HIV Infections; Humans; Immunologic Deficiency Syndromes; Killer Cells, Natural; Life Style; Male; Methadone; Middle Aged; Naloxone; Narcotics; Neurosecretory Systems; Opioid-Related Disorders; Stereoisomerism; T-Lymphocyte Subsets

The effect of acute (1 day) or subchronic (25 days) treatment with delta 9-tetrahydrocannabinol (THC), the major psychoactive constituent of marihuana, on plasma norepinephrine (NE), epinephrine (E), corticosterone, beta-endorphin (beta-end), and splenic natural killer (NK) cell activity of the rat was studied. Groups of animals received subcutaneously, either THC in corn oil + saline (3 mg THC/kg); oil + saline; or THC + naloxone (2 mg naloxone/kg and 3 mg THC/kg). Acute injection of THC with or without naloxone did not significantly change plasma levels of NE, E corticosterone, beta-end, or the NK cell activity. However, subchronic treatment with THC significantly reduced plasma levels of NE, E, corticosterone, and NK cell activity, compared to controls. The plasma beta-end levels were significantly elevated in the THC-treated animals. In the THC + naloxone group of animals, the plasma hormone levels (corticosterone and beta-end) were similar to control levels and the NK cell activity was significantly higher than in THC-treated animals. These results indicate that subchronic exposure to THC results in suppression of splenic NK cell activity. The interaction of THC with the endogenous opiate system appears to be a contributing factor leading to the NK cell suppression in rats. A direct suppressive action of THC or its metabolites on the NK cell is not ruled out by this study.

Topics: Animals; beta-Endorphin; Catecholamines; Corticosterone; Dronabinol; Endorphins; Immunologic Deficiency Syndromes; Injections, Subcutaneous; Killer Cells, Natural; Male; Naloxone; Rats; Rats, Inbred Strains; Spleen