naloxone and Leukocytosis

Studies examined the role of growth hormone, catecholamines, and beta-endorphins in changes in natural killer cell activity, subtypes of blood mononuclear cells, and leukocyte concentration in response to hot water immersion in humans. The response of leukocytes and neutrophils to 2 hours of hot water immersion and simultaneous administration of propranolol, somatostatin, naloxone, or isotonic saline are reported.

Topics: Adrenergic beta-Antagonists; Adult; Body Temperature; Endorphins; Fever; Growth Hormone; Hormone Antagonists; Hot Temperature; Humans; Immersion; Killer Cells, Natural; Leukocytes; Leukocytes, Mononuclear; Leukocytosis; Male; Naloxone; Narcotic Antagonists; Neutrophils; Propranolol; Sodium Chloride; Somatostatin; Water

The antidotal effects of antiinflammatory agents, inhibitors of bioamine syntheses, an opioid antagonist and other pharmacological agents on lethal toxicity, leukocytosis and ear inflammation, were investigated in mice subcutaneously administered or topically exposed to T-2 toxin, a trichothecene mycotoxin of Fusarium species. The acute lethal toxicity of T-2 toxin was reduced by administration of the steroidal anti-inflammatory agents, prednisolone and dexamethasone, and prolongation of survival times was demonstrated with an antihistaminic agent, diphenhydramine, and an opioid antagonist, naloxone. Prednisolone also antagonized leukocytosis and the increment of ear weight caused by T-2 toxin. These findings suggest that the action site(s) of steroidal anti-inflammatory agents is involved in the development of the toxic actions of T-2 toxin, and the implications of the results with bioamines and opioids are also discussed.

Topics: Animals; Anti-Inflammatory Agents; Antimetabolites; Dexamethasone; Edema; Lethal Dose 50; Leukocytosis; Male; Mice; Naloxone; Prednisolone; Sesquiterpenes; T-2 Toxin