UMLS:C0011570 - FACTA Search

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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy of once-daily bisoprolol (10 mg) and atenolol (100 mg) was assessed in 19 patients with stable angina, using a double-blind randomized crossover protocol and computer-assisted treadmill exercise testing with continuous monitoring of leads CM5 and CC5, the test being carried out 22-24 h after the last dose. The mean +/- SEM exercise time on placebo was 6.5 +/- 0.4 min increasing to 7.8 +/- 0.5 min on bisoprolol (p less than 0.02) and 8.6 +/- 0.6 min on atenolol (p less than 0.001). The increase in exercise time with atenolol was significantly greater than with bisoprolol (p less than 0.02). The time to 1 mm ST-depression in CM5 and CC5 was also prolonged significantly with both drugs compared to placebo, but with no difference between the two active treatments. The mean resting heart rate of 84 +/- 4 beats/min decreased to 63 +/- 2 beats/min on bisoprolol (p less than 0.001) and 64 +/- 2 beats/min on atenolol (p less than 0.001) with a significant decrease in the peak exercise heart rate seen with both drugs (p less than 0.001). The peak rate-pressure product (beats/min X mm Hg X 10(-2)) was 175 +/- 8 after placebo, 146 +/- 7 (p less than 0.001) after bisoprolol and 149 +/- 5 (p less than 0.01) after atenolol. One patient was withdrawn because he suffered a myocardial infarction. After completion of the crossover phase, 18 of the patients were prescribed bisoprolol 10 mg once a day for 6 weeks. Twelve patients were treated for 12 weeks. An exercise test was performed at the end of each 6-week period. The effects of bisoprolol on all parameters were maintained. In conclusion, bisoprolol is an effective antianginal agent, comparable in efficacy and duration of action with atenolol, and is suitable for once daily administration.
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PMID:Management of chronic stable angina with once-daily bisoprolol or atenolol and long-term efficacy of bisoprolol. 243 87

Bretylium tosylate and bethanidine sulfate were studied in two models of experimental myocardial ischemia. In anesthetized dogs, left anterior descending coronary artery occlusion during rapid atrial pacing (180-200 min-1) produced ventricular tachycardia and fibrillation within 5 min in 9 of 11 dogs studied. In all cases, arrhythmias were preceded by and appeared to be temporally related to progressive fractionation and delay of electrograms recorded from the ischemic zone. In four dogs, bretylium (10 mg/kg) did not alter the time course of electrogram changes nor the time to onset of arrhythmia. However, in five dogs bethanidine (10 mg/kg) markedly exacerbated conduction changes in the ischemic zone and decreased the time to onset of ventricular arrhythmias (173 +/- 35 vs. 262 +/- 34 s control, mean +/- SEM, p less than 0.05). Bethanidine administration also facilitated ischemia-induced ventricular tachycardia and fibrillation in two dogs that did not exhibit ischemia-induced arrhythmias before receiving the drug. In isolated perfused rabbit hearts, global ischemia produced conduction slowing, depolarization of resting membrane potential, and decreases in amplitude and Vmax that were reproducible in serial 10 min ischemic episodes. Bretylium (10 mg/L) did not affect these parameters under either perfused or ischemic conditions. Although bethanidine (10 mg/L) also did not affect these parameters during perfusion, conduction slowing and depression of Vmax during ischemia were accelerated without affecting the time course of change in resting membrane potential. Both bretylium and bethanidine prolonged action potential duration under perfused conditions, but after 10 min of ischemia this effect was no longer evident. The results demonstrate that differences in the electrophysiologic effects of bretylium and bethanidine are markedly accentuated in the setting of acute ischemia. Although both these agents have been demonstrated to have antifibrillatory effects in other experimental settings, under the conditions of this study, bretylium failed to protect against ischemia-induced arrhythmias and acute bethanidine administration produced a proarrhythmic effect in association with an exacerbation of ischemia-induced conduction changes.
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PMID:Ischemia-induced conduction delay and ventricular arrhythmias: comparative electropharmacology of bethanidine sulfate and bretylium tosylate. 247 95

The direct and reflex-mediated components of the cardiovascular response to administration of neuro-peptide Y (NPY) in intact conscious rabbits were determined by studies with cardiac beta adrenoceptor and vagal blockade, and during total autonomic blockade. Cardiac pacing was used to prevent bradycardia, and sinoaortic denervation (SAD) was used to remove afferent baroreflex input. In control animals, NPY (10 micrograms/kg bolus i.v.) caused arterial pressure to increase from 77.4 +/- 1.5 mm Hg (mean +/- SEM) to a maximum of 91.4 +/- 1.6 mm Hg (p less than 0.05). This pressor response was independent of autonomic effectors but was buffered by arterial baroreflexes. The fall in heart rate (HR) from 281 +/- 14 to 252 +/- 18 beats/min (p less than 0.05) was mediated in part through baroreceptor-dependent changes in cardiac autonomic efferent activity, but was in part independent of autonomic neural mechanisms. Peak left ventricular (LV)dP/dt fell from 5,551 +/- 342 to 4,182 +/- 394 mm Hg/s (p less than 0.05) following NPY in control rabbits. This reduction was maintained during pacing and following SAD, and was caused partly by a withdrawal of cardiac beta-adrenergic tone and partly through a non-beta-mediated myocardial depression. Small changes in cardiac output (CO) and in LV end-diastolic pressure (LVEDP) after NPY were secondary to bradycardia. Total autonomic blockade did not impair the NPY-induced rise in total peripheral resistance (TPR), suggesting a direct vasoconstrictor action that was independent of neural mechanisms.
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PMID:Effects of neuropeptide Y on the heart and circulation of the conscious rabbit. 248 Nov 83

Canine and human coronary arteries were studied in organ baths to compare the responses to acetylcholine and serotonin in the two species. The human coronary rings were isolated from seven patients without cardiac disease (mean age 15 years, range 7-20). In one set of experiments canine and human preparations were incubated with phentolamine, propranolol and ketanserin (all at 1 mumol.litre-1 concentration) and precontracted with prostaglandin F2 alpha (PGF2 alpha 1-2 mumol.litre-1). Acetylcholine (0.1-10 mumol.litre-1) and serotonin (0.1-100 mumol.litre-1) relaxed canine preparations dose dependently, the maximum responses (expressed as % of depression of PGF2 alpha response) being 84 (SEM 6)% (n = 9) and 51(5)% (n = 6) respectively. In the same experimental conditions, acetylcholine and serotonin failed to relax the human coronary rings (n = 11) while substance P and bradykinin induced relaxations of 72(4)% (n = 11) and 66(7)% (n = 11) of PGF2 alpha response respectively. In another set of experiments, dose-contraction curves were constructed for acetylcholine or serotonin (in presence of phentolamine and propranolol). On human rings with endothelium, methylene blue (10 mumol.litre-1), a non-specific inhibitor of endothelium derived relaxing factor (EDRF), potentiated these dose-contraction curves: markedly for serotonin, the EC50 decreasing from 1.2(0.2) to 0.22(0.08) mumol.litre-1 (n = 11, p less than 0.01) with a significant increase in the maximal response); and slightly for acetylcholine, EC50 decreasing from 0.84(0.11) to 0.40(0.13) mumol.litre-1 (n = 10, p less than 0.05) without significant change in the maximal response.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of responses to acetylcholine and serotonin on isolated canine and human coronary arteries. 248 33

Of the researches on periodontal diseases, the changes occurred in the vasculature of peridontal membrane and the surrounding alveolar bone there-to-fore attracts much attention. In order to induce an experimental occlusal trauma, composite resin was added on the occlusal surfaces of mandibular second and third premolars of dogs to raise the bite for a period of time, followed by injection of methacrylate resin (MERCOX) into inferior alveolar artery and dissolution of soft tissues by protainase and examined under the scanning electron microscope (SEM, JEOL 35 C). The results are as follows: After 14 days, a wide range of avascularized area was observed on resin cast of periodontal membrane. The surface of alveolar bone on which the vasculature disappeared did not show resorption process. However, the surface of alveolar bone next to the periodontal vasculature showed undergoing a direct bone resorption. After 30 days, the vasculature of periodontal membrane underwent a morphological change and turned out to appear as a mesh-like vascular network. Certain avascularized regions was observed over the alveolar bone on margin region and cervical region, and it was circumscribed by a vasculature with glomerule-like loops. This vasculature was suspected originating from underlying alveolar bone marrow and connected with the residual vasculature of periodontal membrane. After 60 days, vasculature of periodontal membrane facing teeth appeared quite resemblance with that of health periodontal membrane. Those next to the alveolar bone, however, showed enlargement. In this period, avascularized area was not observed. After 90 days, the vasculature in periodontal membrane lost its original two-layered arrangement and replaced by the irregular arrayed bundle-like vasculature. Longitudinally arrayed mesh like vasculature was observed in certain region of periodontal vasculature. After 180 days, bundle-like vessels arrayed as an ellipse pattern. Also, resorption process could be observed on the surface of alveolar bone and interradicular septum. Experimental study of occlusal trauma on dentition clearly indicated that teeth were showed a mobility in vertical direction and that the vasculature of periodontal membrane were showed depression and elongation for a period of time. It could not show an apposition where were showed by the experimental depression and elongation, so it was only showed the expansible periodontal membrane space by resorption of alveolar bone.
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PMID:[Changes of periodontal vasculature and alveolar bone on the occlusal trauma]. 248 55

The surface structure of the connective tissue papillae (CP) of Suncus murinus tongue was observed by SEM after fixing with Karnovsky's fixative and removal of the epithelial cell layer with 3N or 8N HCl. On the surface of the slender conical tongue, there are densely distributed filiform papillae among which fungiform papillae are seen sporadically. A pair of vallate papillae are situated in the posterior region of the tongue. Filiform papillae appear somewhat different externally depending on the dorsal surface of the anterior tongue. At the tip of the tongue, filiform papillae are of a slender conical shape and have a slight depression in the anterior basal portion. The CP of these is seen as a spherical protrusion on which a shallow groove runs in the anteroposterior direction. In the middle region, somewhat large filiform papillae contain CP having one or two small round head-like structures on each spherical protrusion. These head-like structures are increased in number in the posterior region. In the most posterior region of the anterior tongue, there are distributed large filiform papillae having several slender protrusions that surround a basal anterior depression. These large branched filiform papillae have a glove finger like CP. Small conical filiform papillae are distributed in the posterior marginal region of the anterior tongue which have CP of a horse-shoe like protrusion that opens in the anterior direction. Spherical fungiform papillae have CP which are thick columnar in shape with many lateral thin folds running vertically and having a round depression on the top of each. CP of the vallate papillae appear as a beehive like structure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Three dimensional structure of the connective tissue papillae of the tongue in Suncus murinus]. 251 78

The neuromuscular and cardiovascular effects of doxacurium chloride (BW A938U) were evaluated in 27 children (2-12 yr) anaesthetized with 1% halothane and nitrous oxide in oxygen. In nine children the incremental technique was used to establish a cumulative dose-response curve by train-of-four stimulation. The remaining children received either 30 or 50 micrograms kg-1 of the drug as a single bolus. The median ED50 and ED95 of doxacurium in children were 19 and 32 micrograms kg-1, respectively. No clinically significant change in heart rate or arterial pressure occurred. Following doxacurium 30 micrograms kg-1 and 50 micrograms kg-1, recovery to 25% of control occurred in 25 (SEM 6) and 44 (3) min, respectively. The recovery index (25-75% of control) was 27 (2) min. The duration of action of doxacurium is similar to that of tubocurarine and dimethyl-tubocurarine in children. Compared with adults, children seem to require more doxacurium (microgram kg-1) to achieve a comparable degree of neuromuscular depression, and they recover more rapidly.
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PMID:Neuromuscular and cardiovascular effects of doxacurium in children anaesthetized with halothane. 252 89

Mivacurium is a new short-acting competitive neuromuscular blocking agent. Infusion requirements for the maintenance of a stable 90-99% muscle twitch depression were determined in 28 children anaesthetized with nitrous oxide and 1% halothane (inspired) in oxygen or nitrous oxide in oxygen and opioid. Neuromuscular block was assessed by monitoring the force of contraction of the adductor of the thumb during train-of-four (TOF) stimulation at 0.1 Hz. Infusion rate and twitch depression were analysed from 15 to 75 min and from 75 to 135 min after the start of the infusion. In the first period of evaluation, the mean infusion requirement was 10.4 (SEM 0.92) micrograms kg-1 min-1 during the halothane anaesthesia and 13 (1.4) micrograms kg-1 min-1 during the opiod anaesthesia (P less than 0.05). This difference was present also during the second 60-min period. There was no significant correlation between infusion rates required to maintain greater than 90% depression of the first twitch (T1) of the TOF and plasma cholinesterase concentrations. Regardless of the anaesthetic regimen, children recovered rapidly after discontinuing the infusion. The recovery index (25-75% recovery of T1) for all patients was 5.4 (0.57) min with no significant differences between the groups.
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PMID:Continuous infusion of mivacurium in children. 253 33

Starvation for 24 h causes a striking fall in glutathione content from 3.19 +/- 0.27 to 1.88 +/- 0.14 (X +/- SEM) mumol/g tissue and of GGT activity from 31.75 +/- 4.17 to 19.49 +/- 3.13 (X +/- SEM) nmol/min/mg protein in the homogenate from whole mucosa of the upper small intestinal segments. This was associated with a significant increase in GSH-Px activity and the content of lipid peroxides (measured by the thiobarbituric assay). On semi-synthetic iron-supplemented diet the activities of GSH-T and GGT were significantly decreased as compared with crude diet. On semisynthetic iron-depleted diet GSH-T and GGT activities were further depressed, but this was accompanied with an additional depression of GSH, glutathione reductase (GSSG-R), and glutathione peroxidase (GSH-Px) activities and lipid peroxide concentrations. Food deprivation significantly lowers the mucosal GSH-content and could lead to a destabilization of this system presumably by increased oxidative stress. As compared to normal "crude" diet, semisynthetic diets and oral iron depletion have been shown to cause a depression of the intestinal GSH system. As a consequence of these effects, the resistance of the small intestinal mucosa toward exogeneous dietary toxins might be reduced.
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PMID:Glutathione and its related enzymes in the small intestinal mucosa of rats: effects of starvation and diet. 256 68

We compared the ability of 3 alpha 2-adrenoreceptor antagonists, idazoxan (0.05 mg/kg), tolazoline (2 mg/kg), and yohimbine (0.2 mg/kg) to reverse xylazine (0.3 mg/kg)-induced respiratory changes and CNS depression in 6 ewes. Once weekly, each ewe was given a random IV treatment of xylazine, followed in 5 minutes by either an antagonist or 0.9% NaCl solution. Xylazine alone caused recumbency for 54.2 +/- 5.3 minutes (mean +/- SEM). Xylazine also increased respiratory rate and decreased PaCO2 for at least 45 minutes, but did not significantly change arterial pH or PaCO2. Idazoxan and tolazoline were equally effective in reversing the respiratory actions of xylazine; however, yohimbine was less effective in reducing the respiratory rate and was ineffective in antagonizing the decreased PaO2. Idazoxan and tolazoline decreased the duration of xylazine-induced recumbency to 6.3 +/- 0.6 and 9.5 +/- 2.3 minutes, respectively, whereas yohimbine did not significantly change this effect of xylazine. Thus, at the dosages studied, idazoxan and tolazoline appeared to be more effective than yohimbine in reversing the respiratory and CNS depressant actions of xylazine in sheep.
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PMID:Effects of idazoxan, tolazoline, and yohimbine on xylazine-induced respiratory changes and central nervous system depression in ewes. 257 91

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