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physostigmine salicylate/vômito
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A multicenter double-blind study of controlled-release physostigmine for the treatment of symptoms secondary to Alzheimer's disease. Physostigmine Study Group.
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OBJECTIVE
A multicenter trial to evaluate the efficacy of controlled-release physostigmine salicylate, a cholinesterase inhibitor, was conducted in 1,111 mild-to-moderate Alzheimer's disease (AD) subjects.
METHODS
During dose titration, subjects received 18, 24, or 30 mg of physostigmine or placebo
Physostigmine fails to reverse clinical, psychomotor, or EEG effects of lorazepam.
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Physostigmine salicylate (2.0 mg) or 0.9% NaCl (2.0 ml) was administered intravenously in a double-blind fashion to adult volunteers in an attempt to reverse the effects of a 0.05-mg/kg dose of lorazepam given intravenously 30 min earlier. No other medication affecting the central nervous system was
Extended-release physostigmine in Alzheimer disease: a multicenter, double-blind, 12-week study with dose enrichment. Physostigmine Study Group.
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BACKGROUND
The efficacy of extended-release physostigmine salicylate, an acetylcholinesterase inhibitor, was evaluated in 850 subjects with mild-to-moderate Alzheimer disease (AD) in a multicenter trial.
METHODS
Subjects initially entered a dose-enrichment phase in which they received 1 week each of
Physostigmine antagonizes ketamine.
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In a random cross-over double-blind trial, the effects of intravenous physostigmine salicylate (2.0 mg) and placebo were observed in seven healthy volunteers 10 minutes after the intravenous administration of 1.5 mg/kg of ketamine. Recovery time was significantly shorter after physostigmine than
Subacute atropine toxicity in a pygmy sperm whale, Kogia breviceps.
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Atropine, an anticholinergic agent commonly used in human and veterinary medicine, is reported to cause toxicity associated with its antimuscarinic action. A juvenile pygmy sperm whale, Kogia breviceps, was treated with atropine in an attempt to relieve symptoms similar to pyloric stenosis, as has
Physostigmine for Alzheimer's disease.
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BACKGROUND
The main pharmacological approach for the treatment of Alzheimer's disease (AD) has been based on the use of agents potentiating cholinergic transmission, particularly by inhibiting acetylcholinesterase (AChE), the enzyme that destroys acetylcholine after it has been secreted into the
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