Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three groups of 6 rats each were given a single dose of 20, 50, or 100 mg/kg phenobarbital. The EEG was recorded for 15 min before and 1, 2, 4, 8 and 24 h after phenobarbital administration. Serum levels of phenobarbital in all rats were assayed at 1, 2 and 4 h. In the 20 mg/kg group, the beta 2 band was significantly increased from 2 to 4 h following phenobarbital administration. In the 50 mg/kg group, the beta 2 band significantly increased from 2 to 8 h (P < 0.01), and the theta band decreased at 8 h (P < 0.01). In the 100 mg/kg group, the beta 2 band was significantly increased during 24 h (P < 0.01) and the theta band was significantly decreased during 2 and 8 h (P < 0.05, P < 0.01). As for phenobarbital concentrations, in all rats, serum phenobarbital levels became gradually higher with time. When serum levels became more than 25 micrograms/ml, the beta 1 and beta 2 bands showed a significant increase. Whereas, above 35 micrograms/ml, theta waves decreased significantly. These results suggest that the significant increase of fast waves resulted from inhibition of reticular activating system and theta waves mainly resulted from depression of the cortex.
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PMID:Relationship between serum levels and fast EEG activities in rats by a single administration of phenobarbital. 616 Sep 94

We have characterized a UDP-GlcNAc:Gal beta-3-GalNAc (GlcNAc----GalNAc) beta-6-N-acetylglucosaminyltransferase from rabbit small intestinal epithelium by using freezing point depression glycoprotein as the acceptor. Optimal enzyme activity was obtained at pH 7.0-7.5, at 3 mM MnCl2, and at 0.08% Triton X-100. Ca2+, Mg2+, and Ba2+ also enhanced enzyme activity. The apparent Michaelis constant was 4.80 mM for freezing point depression glycoprotein, 0.59 mM for periodate-treated porcine submaxillary mucin, 0.49 mM for Gal beta 1----3 GalNAc alpha Ph, and 1.03 mM for UDP-GlcNAc. No enzyme activity was observed when asialo ovine submaxillary mucin was used as the acceptor. The 14C-labeled oligosaccharide obtained by alkaline borohydride treatment of the product was shown to be a homogeneous trisaccharide by compositional analysis, Bio-Gel P-4 gel filtration, and high-performance liquid chromatography. The structure of the trisaccharide was identified as Gal beta 1----3-(GlcNAc beta 1----6)GalNAc-H2 by (a) identification of 2,3,4,6-tetramethyl-1,5-diacetylgalactitol and 1,4,5-trimethyl-3,6-diacetyl-2-N-methylacetamidogalactitol by gas-liquid chromatography-mass spectrometry and (b) the complete cleavage of the newly formed glycosidic bond by jack bean beta-hexosaminidase. The structure of the trisaccharide was confirmed by 1H nuclear magnetic resonance (270 MHz) and also by periodate oxidation of the trisaccharide followed by NaBH4 reduction, 4 N HCl hydrolysis, a second NaBH4 reduction, and the identification of threosaminitol on an amino acid analyzer. By acceptor competition studies, the enzyme activity was shown to be a much N-acetylglucosaminyltransferase. We postulate that this glycosyltransferase may play a key role in the regulation of mucin oligosaccharide synthesis.
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PMID:Mucin biosynthesis: characterization of rabbit small intestinal UDP-N-acetylglucosamine:galactose beta-3-N-acetylgalactosaminide (N-acetylglucosamine----N-acetylgalactosamine) beta-6-N-acetylglucosaminyltransferase. 623 49

Nadolol, a new nonselective beta 1 and beta 2 adrenergic blocking agent, has a plasma half-life of 17 to 23 hours. We studied 37 volunteers with stable angina pectoris who had five or more episodes of pain per week and who also had a 1 mm or greater ST segment depression 80 msec past the J point during a Bruce protocol treadmill test. An eight-week placebo controlled run-in period preceded double-blind randomization to nadolol administered once per day (17 patients) or identical appearing placebo for four weeks (20 patients), after which an exercise test was done. Diaries for pain episodes and nitroglycerin consumption were kept. Exercise tests were performed 24 hours after the last nadolol or placebo dose. Episodes of pain per week were reduced 59.8 percent after nadolol and 28.2 percent after placebo (P less than .01). Nitroglycerin consumption after nadolol was reduced 66.8 percent while after placebo it was reduced 36.2 percent (P less than .05). Resting and peak heart rates and peak rate-pressure products showed typical reductions due to beta-blockade 24 hours after nadolol compared with stability of these during placebo, all P less than .001. Exercise time after nadolol increased 42.2 percent, which was more than the 14.5 percent increase after placebo (P less than .05). Exercise work after nadolol increased 64.7 percent, greater than the 22 percent increase after placebo (P less than .05). Mean ST segment depression at end of exercise was little changed before and after treatment in both groups, reflecting consistency of effort. Improvement in symptoms and work capacity associated with nadolol significantly exceeded the placebo group responses. Unlike other available agents of this class, a single daily dose of nadolol produced therapeutically effective 24-hour beta-blockade in patients with disabling angina pectoris.
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PMID:Comparison of nadolol, a new long-acting beta-receptor blocking agent, and placebo in the treatment of stable angina pectoris. 679 83

1 Pindolol is a non-selective beta-adrenoceptor blocking agent; its affinity to adrenoceptors in guinea pig atria (beta 1) is not significantly different from that in guinea pig trachea (beta 1 + beta 2) and canine vascular smooth muscle (beta 2). 2 Pindolol displays a striking diversity of agonist activities in isolated tissues. Stimulant effects correspond to 40--50% of the maximum effects of isoprenaline in isolated kitten atria and guinea pig trachea and to only 10% in guinea pig atria. Effects in canine isolated mesenteric vessels are those of a full agonist, maximum responses equaling those of isoprenaline. These findings suggest that the stimulant effects of pindolol are exerted principally on beta 2-adrenoceptors. 3 Cardiac stimulation produced by pindolol in the dog is sufficient to compensate for the cardiac depression resulting from blockade of beta-adrenoceptors in the heart. Reductions in cardiac output and compensatory increases in total peripheral resistance do not occur or are much smaller than those produced by beta-adrenoceptor blocking agents lacking sympathomimetic activity. 4 Pindolol-induced relaxation of bronchial smooth muscle prevents or minimizes the bronchoconstrictor effects of injected spasmogens in the cat. 5 Pindolol has marked vasodilator activity, small doses reducing femoral and mesenteric vascular resistance by approximately 30%. Doses comparable to those used in hypertensive patients lower blood pressure by 20 mmHg in non-anaesthetized dogs.
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PMID:Pindolol--the pharmacology of a partial agonist. 704 8

Thirty patients with stable angina have been undergone a multistage treadmill test, after a single oral dose of 100 mg of Atenolol, a beta 1 . selective blocking agent, in comparison to a previous test carried out after an identical looking placebo tablet. After placebo all the patients showed ischemic ST segment response (ST depression greater than 1 mm), 25 of them interrupting the test because of anginal pain (20 patients), or of ST depression greater than 3 mm (3 patients), or of ventricular ectopics (one patient), or of fatigue (one patient). After Atenolol 10 patients completed the planned test, 7 of them without ischemic changes of ST. 27 patients (90%) showed increased working capacity with significant reduction of heart-rate (FC), systolic blood pressure (PAS) and their product and of ST depression, either before and during and at the end of exercise. The recovery time of ischemic ECG change has been significantly reduced. The observed increased working capacity is attributed to the reduced myocardial O2 consumption expressed from the reduction of the product FC x PAS. Nevertheless at the end of exercise test after beta-blocking drug this product didn't reach the threshold value at which the test was interrupted in the first test after placebo. The authors discuss the possible cause of this effect of beta-blocking drugs, which could be attributed to a reduction of coronary blood flow and/or to an increased myocardial tension because of increased end diastolic ventricular volume. However the Authors outline that the per cent increases of FC, PAS, and FC x PAS have not been reduced by the Atenolol, unlike their absolute values, at the threshold of angina: the ischemic reveals itself at same levels of per cent increase of the factors of O2 myocardial consumption, the later reaching of threshold values depending on the lower starting values. The advantages of Atenolol as regards the other beta-blocking drugs (better acceptability, stability and duration of action) are outlined too.
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PMID:[Evaluation by exercise test of effects of a single oral dose of atenolol in patients with stable angina (author's transl)]. 704 18

Regional myocardial function was assessed by multidirectional echocardiography from eight standardized segments around the left ventricle. Thirty-six subjects (healthy, severe angina pectoris, or acute myocardial infarction) were studied 15 minutes either after the beta 1-selective beta-blocking drug metoprolol had been administered in total doses of 2 and 10 mg intravenously or after pindolol, a beta blocker with intrinsic sympathomimetic activity (ISA), in total doses of 0.2 and 1.0 mg intravenously had been given. Metoprolol and pindolol reduced rate-pressure product (p less than 0.001 each), heart rate (p less than 0.001), and systolic blood pressure (p less than 0.05 to 0.001) in almost the same way. In patients with acute myocardial infarction, 0.2 mg pindolol improved ST segments by 33% and 2 mg metoprolol by 18%. Left ventricular diameter increased (p less than 0.001) and ejection fraction decreased (p less than 0.05) after metoprolol but not after pindolol. Pindolol did not reduce wall motion amplitudes of healthy myocardial segments, while metoprolol did ( p less than 0.01). The overall contractile function of the left ventricle is characterized by composite segmental amplitudes from both ischemic and healthy ventricular regions. In ischemic hearts this function remained unchanged after metoprolol but improved markedly after pindolol (p less than 0.005). Thus, while intravenous pindolol and metoprolol produced equal reductions in rate-pressure product, pindolol, a beta-adrenergic-blocking drug with intrinsic sympathomimetic activity, evoked less cardiac depression and thus provided a cardiac safety factor not afforded by the beta- 1-selective metoprolol.
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PMID:Cardiac safety of acute beta blockade: intrinsic sympathomimetic activity is superior to beta-1 selectivity. 710 33

The pharmacokinetics and pharmacodynamics of d-tubocurarine (dTc) were determined in neonates (0-2 months, n = 7), infants (2-12 months, n = 7), children (1-12 years, n = 9), and adults (12-30 years, n = 8) during 70% nitrous oxide, 0.58 MAC halothane anesthesia. dTc was administered by infusion, while blood for determination of plasma dTc concentrations was obtained, and the EMG of the adductor pollicis recorded. The plasma dTc concentration at which 50% depression of EMG twitch height occurs (Cpss(50)) was 0.18 +/- 0.09 micrograms/ml in neonates, and 0.27 +/- 0.06 micrograms/ml in infants, both significantly lower than the values of 0.42 +/- 0.14 and 0.53 +/- 0.14 micrograms/ml for children and adults, respectively. The steady-state distribution volume (Vdss) was 0.74 +/- 0.33 l/kg in neonates, significantly greater than the values of 0.52 +/- 0.22, 0.41 +/- 0.12, and 0.30 +/- 0.10 l/kg in infants, children, and adults, respectively. The elimination half-life (t beta 1/2) was 174 +/- 60 min in neonates, significantly longer than the values of 90 +/- 23 and 89 +/- 18 min in children and adults, respectively. Plasma clearance did not differ with age. We also determined D50, the product of Vdss and Cpss(50). D50, the quantity of drug present at steady-state to produce 50% paralysis, did not differ between groups. The authors conclude that during comparable nitrous oxide-halothane anesthesia, neonates and infants have an increased sensitivity to dTc, as determined by CPss(50). However, because of the larger Vdss in younger patients, dose size should not differ with age. In addition, because of the longer t beta 1/2 in neonates, second and subsequent doses should be required at less frequent intervals.
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PMID:Pharmacokinetics and pharmacodynamics of d-tubocurarine in infants, children, and adults. 711 42

Maximal exercise performance by eight healthy male subjects was tested after one week of medication with slow-release metoprolol 200 mg/d (metoprolol-SR), atenolol 200 mg/d or placebo, in a double blind crossover trial. The maximal working capacity was significantly decreased after atenolol and metoprolol-SR. Plasma glucose and FFA concentrations during the exercise test did not change: either after placebo therapy or after beta-blockade. The anerobic threshold did not change after beta-blockade, but the changes in lactate due to the exercise were less after beta-blockade. Neither beta-blocker affected the exercise-induced alteration in airway resistance. Both drugs caused a small but significant ventilatory depression at rest and at 75% of maximal exercise. It is concluded that the limiting factor in maximal exercise performance after beta 1-adrenergic blockade does not lie in oxygen transport to the working muscles via ventilation and the circulation, but is most probably due to anaerobic metabolism.
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PMID:Metabolic aspects of maximal exercise performance after slow release metoprolol and after atenolol. 717 99

Chronic ingestion of caffeine by male NIH Swiss strain mice leads in about 3 days to a significant increase in A1-adenosine, nicotinic and muscarinic receptors, and a significant decrease of beta 1-adrenoceptors in cerebral cortical membranes. Plasma levels of caffeine in the chronically treated mice range from 0.70 to 5.7 micrograms/ml. The changes in receptors reverse after withdrawal of caffeine within 7 days. An increase in nitrendipine binding sites, associated with L-type calcium channels, also occurs within 4 days and has reversed in 7 days after withdrawal. There is no change in the levels of striatal nicotinic receptors of D2-dopamine receptors, nor of [3H]cocaine binding to dopamine uptake sites. Levels of opioid receptors are either increased (delta) or unaltered (mu, kappa). sigma-Receptors are unaltered. Stimulations of striatal adenylate cyclase by forskolin, dopamine and NECA are not significantly affected after chronic caffeine ingestion. The adenosine agonist, NECA, reverses the amphetamine-elicited increases in locomotor activity and partly reverses the cocaine-elicited increases. The NECA dose-response curve is multiphasic (depression, stimulation and then depression) versus amphetamine in control mice, but only depressant versus amphetamine in chronic caffeine mice, while being multiphasic versus cocaine in both control and chronic caffeine mice. NECA reverses the stimulation of locomotor activity elicited by the muscarinic antagonist, scopolamine, and is more effective in the chronic caffeine mice. The behavioral depressant effects of the muscarinic agonist, oxotremorine, are not markedly altered after chronic caffeine ingestion.
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PMID:Effects of chronic caffeine on adenosine, dopamine and acetylcholine systems in mice. 762 82

The purpose of this study was to examine the role of beta-adrenergic receptors in an animal model of stress-induced behavioral depression. beta-Adrenergic receptors in several brain regions and leukocytes of rats were determined by receptor binding techniques using 125I-cyanopindolol (cyp) as ligand and propranolol as displacer for total beta-adrenergic receptors, and ICI 86,406 for beta 1- and ICI 118,551 for beta 2-adrenergic receptors. We observed that the maximum number of binding sites (Bmax) and the apparent dissociation constant (Kd) of 125I-cyp binding to total beta-adrenergic receptors were increased in hippocampus of stressed rats with escape deficits (48 h after training) as compared to control rats. This increase was due to an increase in Bmax and Kd of 125I-cyp binding to beta 1-adrenergic receptors but not to beta 2-adrenergic receptors. There was no significant difference in beta 1-adrenergic receptors in cortex and cerebellum or beta 2-adrenergic receptors in hippocampus, cortex, cerebellum, or leukocytes of stressed (48 h after training) rats with escape deficits as compared to control rats. Interestingly, it was observed that beta 1- and beta 2-adrenergic receptors in various brain regions (cortex, cerebellum, and hippocampus) and beta 2-adrenergic receptors in leukocytes of stressed rats (10 days after training) were not significantly different from control rats, although escape deficits were still present. These results suggest that abnormalities in adrenergic neurotransmission are associated with an upregulation of beta 1-adrenergic receptors, which in turn may be involved in the early stages of behavioral deficits caused by uncontrollable shock.
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PMID:Beta-adrenergic receptor subtypes in stress-induced behavioral depression. 766 50


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