Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of the opiate antagonist naloxone on both the neurological deficit and regional cortical blood flow after middle cerebral artery occlusion in the cat was investigated. In animals with mild symptoms, naloxone did not consistently produce a significant behavioral effect. In all cats with neurological deficits, including hemiplegia or severe hemiparesis, 2 mg/kg naloxone administered intravenously 4 h after the ischemic lesion produced a reversal of neurological symptoms. This effect began within 2 min following naloxone injection and lasted for approximately 20 min. Animals were then anesthetized and cortical blood flow was measured by the hydrogen clearance method. Average cortical blood flow on the side of the occlusion was 50% that of the control side. Naloxone produced a significant additional decrease of 19.5% in cortical blood flow in the ischemic hemisphere, whereas no effect on blood flow on the control side was noted. Thus, although naloxone appears to temporarily reverse the severe neurological deficits resulting from middle cerebral artery occlusion in the cat, this effect appears to be accompanied by a decrease in local blood flow to the ischemic cortex.
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PMID:Focal cerebral ischemia in the cat: effect of naloxone on cortical blood flow and neurological deficit following middle cerebral artery occlusion. 345 50

The proximal left M1 and the common trunk of A2 were clipped in 12 adult dogs. Naloxone was injected after placing the clips onto 6 dogs. Neither the systemic blood pressure nor the local cerebral blood flow were influenced by naloxone. In another group of 6 dogs with chronic right hemiplegia, naloxone proved passably effective in improving the hemiplegia. Eight patients with neurological deficits of various etiologies were administered levallorphan. The improvement in motor performance and/or elevation of mental activity was observed more or less in all but 2 of the patients. It was considered that the effect of opiate antagonists is based partially on the facilitation of synaptic transmission exaggerated by the arousal response.
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PMID:Opiate-antagonist reversal of neurological deficits--experimental and clinical studies. 377 54

The effects of an opiate agonist (morphine) and antagonist (naloxone) on neurologic function in conditions of acute and subacute focal cerebral ischemia were tested in a baboon model. Fourteen baboons (Papio papio) underwent unilateral transorbital microsurgical occlusion of the middle cerebral artery (MCA). Blood pressure, heart rate and core temperature were monitored continuously; frequent arterial blood gas measurements were made. Cardiac output, cardiac filling pressures, and regional cerebral blood cross-flow were measured in selected baboons. Naloxone administered intravenously consistently reversed hemiparesis and hemiplegia in all baboons for as long as they lived (4 h to 8 days postocclusion). Morphine administered intravenously converted hemiparesis to hemiplegia; this effect was naloxone-reversible. There were no significant changes in any parameter measured after the administration of either drug. Phenylephrine (used to elevate mean arterial pressure to 20 mm higher than the highest pressure measured after naloxone administration) and isoproterenol (used to elevate cardiac output to 1 l/min higher than the highest value measured after naloxone administration) produced no change in neurologic function. It appears that naloxone can reverse, and morphine exacerbate, focal ischemic neurologic deficits produced in baboons by MCA occlusion. The observed changes in neurologic function are not associated with or mediated by alterations in core temperature or cardiopulmonary functions.
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PMID:Naloxone reversal and morphine exacerbation of neurologic deficits secondary to focal cerebral ischemia in baboons. 669 45