Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0600097 (Sedation)
1,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Doses of 0.5 mg and 1.0 mg of the alpha-2-adrenoceptor agonist guanfacine (GUA) and NaCl were administered intravenously (IV) in a randomized order to 18 healthy male subjects. GUA induced growth hormone (GH) secretion in a dose-dependent manner without affecting blood pressure or heart rate or inducing sedation. The effects of GUA 1.5 mg i.v. was compared with those of another alpha-2-adrenoceptor agonist, clonidine (CLON) 150 micrograms i.v. in six other male volunteers. Both alpha-2-agonists increased GH to similar levels. CLON reduced both systolic and diastolic blood pressure levels, whereas GUA reduced only systolic levels. Sedation was significantly more pronounced after CLON. The results suggest that the GUA/GH-test (1.5 mg GUA i.v.) may be an alternative to the CLON/GH-test in neuroendocrine assessment of alpha-2-adrenoceptor sensitivity.
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PMID:Guanfacine as an alpha-2-agonist inducer of growth hormone secretion--a comparison with clonidine. 809 32

The alpha2-adrenergic system is involved in the regulation of food intake in animals but its effects on feeding in humans are unknown. We hypothesized that clonidine administration would stimulate food intake in healthy human subjects. Ten men and 4 women, all physically and psychiatrically healthy, received clonidine 3 microg/kg or placebo, orally, in blinded, balanced, randomized order. Consumption of a liquid test meal was measured; also, serum growth hormone levels were used as a secondary measure of clonidine effects. Visual analog scale ratings of hunger, satiety, and sedation were obtained before, during, and after the test meal. A subset of five subjects also received 1.5 microg/kg clonidine, in addition to the two trials described above. Test meal consumption was greater following placebo than following clonidine. Sedation ratings were substantially higher at all time points after clonidine and correlated with meal consumption (correlation coefficient r = -0.584; p = 0.028). Hunger and satiety ratings did not differ. The 1.5 microg/kg dose did not provide different effects on feeding from that seen with placebo. Contrary to our hypothesis, clonidine did not stimulate food intake in humans. Sedation associated with clonidine administration may have suppressed any effects on feeding.
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PMID:Failure of clonidine to stimulate feeding in healthy humans. 976 66

Clonidine stimulation test is widely used to evaluate growth hormone secretion. Side effects are somnolence (35%) and arterial hypotension (AH) (5%). The aims of this paper were to evaluate the tolerance to this test regarding blood pressure (BP) decrease, sedation and the efficacy of saline resuscitation to prevent AH. BP was measured at basal, 60 and 120 min. Sedation was determined by the Ramsay scale. Patients were divided into two groups: Group 1 (n = 80) received saline resuscitation only upon severe AH (drop of mean BP [MBP] > 20% from initial MBP) and/or postural hypotension; Group 2 (n = 100) received saline resuscitation from the beginning of the test. Both groups presented a significant MBP fall and 75% presented somnolence at 60 min. MBP drop did not correlate with either sedation or the clonidine dose. Group 1 presented more hypotension (59% x 28%) and greater MBP drop at 60 min. Only one patient had an asthma attack. We conclude that the hypotension effects caused by oral clonidine diminish with saline resuscitation since the beginning of the test. This test must have specialized medical support with strict BP evaluation and precocious intervention when needed.
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PMID:[Tolerance of the oral clonidine test in 180 patients: efficacy of the volemic expantion in controlling arterial hypotension]. 1635 73