Neuropharmacological agents modifying endotoxin-induced changes in mice.
A variety of neuropharmacological agents were tested to elucidate how chlorpromazine influenced an endotoxin-induced reaction. The results obtained, particularly with beta-adrenergic blocking agents, reserpine and fusaric acid, suggested that the primary locus of chlorpromazine's action was mediated by peripheral beta-adrenergic receptor blockade. Such a locus is compatible with the low doses of propranolol which suppress the reaction, and with successful treatment of shock with dopamine.
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D000928:Antidepressive Agents / Q000494:pharmacology; D002746:Chlorpromazine / Q000494:pharmacology*; D018492:Dopamine Antagonists; D004731:Endotoxins / Q000037:antagonists & inhibitors / Q000633:toxicity*; D004906:Erythrocyte Count; D006632:Histamine / Q000494:pharmacology; D051379:Mice; D009270:Naloxone / Q000494:pharmacology; D010976:Platelet Count; D011943:Receptors, Adrenergic, beta / Q000187:drug effects; D012701:Serotonin / Q000494:pharmacology
D000319:Adrenergic beta-Antagonists; D000928:Antidepressive Agents; D018492:Dopamine Antagonists; D004731:Endotoxins; D011943:Receptors, Adrenergic, beta; D012701:Serotonin; D009270:Naloxone; D006632:Histamine; D002746:Chlorpromazine