Reversal of neurological deficits by opiate antagonist naloxone after cerebral ischemia in animals and humans.
Stroke induced by a carotid occlusion in gerbils was reversed by intraperitoneal (i.p.) injection of naloxone (1 mg/kg) for up to 30 min. Placebo-treated stroked gerbils died in 48 hr; 40% of gerbils implanted with 10 mg naloxone pellets survived over 2 weeks without neurologic deficit. Intravenous (i.v.) injection of naloxone produced the same transient reversal of hemiplegia in 2 patients with neurologic deficit from cerebral ischemia. These findings suggest the involvement of endorphins and opiate receptors in the pathophysiology of stroke, and suggest the possible clinical use of opiate antagonists in humans in the acute phase of stroke.
D000818:Animals; D002545:Brain Ischemia / Q000150:complications / Q000188:drug therapy*; D005849:Gerbillinae; D006429:Hemiplegia / Q000188:drug therapy* / Q000209:etiology; D006801:Humans; D008297:Male; D008954:Models, Biological; D009270:Naloxone / Q000627:therapeutic use*
D009270:Naloxone