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)

This study was conducted to characterize the mechanisms of hyperglycaemia in exercising sheep. Sheep were run on a treadmill for 45 min (5.5 km h-1, 8% incline) during adrenergic blockade (propranolol or phentolamine mesylate infusions) and during suppression of the rise in glucagon by infusion of somatostatin (SRIF). Propranolol did not alter the glucagon, insulin or glucose responses, except it tended to increase the metabolic clearance of glucose, presumably as a result of blocking the beta-adrenergic inhibition of glucose uptake. Phentolamine mesylate administration was associated with a suppression of the rise in glucagon concentrations, a reversal of alpha-adrenergic inhibition of insulin release and a reduction in glucose appearance during exercise. SRIF prevented the rise in glucagon and reduced insulin concentrations to below resting values. Propranolol and phentolamine mesylate did not alter the glucagon, insulin or glucose response to SRIF. However, SRIF prevented the insulin rise that occurred during phentolamine administration. The increment in glucose appearance produced in response to exercise was the same for SRIF, plus phentolamine mesylate and phentolamine mesylate in the first 25 min of exercise, but was significantly less than in the controls. During the last 20 min of exercise, glucose appearance was not significantly different from the control for any of the groups. The depression by SRIF and alpha-adrenergic blockade of the increment in glucose appearance due to exercise was associated with an impairment of the glucagon response. It appears, therefore, that glucagon may stimulate glucose production early in exercise in sheep directly, as well as by having a permissive effect.
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PMID:Effects of somatostatin and adrenergic blockade on glucagon, insulin and glucose in exercising sheep. 612 38

The transuterine potential difference (p.d.) generated by the endometrium was measured in vivo in anaesthetized, ovariectomized rats treated with 10 micrograms oestradiol-17 beta each day for 3 days. Intravenous injection of adrenaline induced transient hyperpolarization of the p.d.; sigmoid dose-dependency was observed over the range 2-40 micrograms/kg. Pre-treatment of the rats with syrosingopine shifted the dose-response curve to the left (enhancement) while combined propranolol (800 micrograms/kg) and phentolamine (800 micrograms/kg) shifted the dose-response curve to the right (depression). Isoprenaline gave similar quantitative changes in the p.d. in vivo which displayed a similar time course and sigmoid dose-dependency. Propranolol alone (800 micrograms/kg) shifted this dose-response curve significantly to the right. Addition of adrenaline or isoprenaline to the serosal solution bathing uteri incubated in vitro after removal from oestradiol-treated rats induced changes in endometrial bioelectric activity that exhibited sigmoid dose-response curves for the transuterine p.d. and short-circuit current (Isc). Propranolol significantly shifted the dose-response curves for adrenaline to the right. Only adrenaline caused small but significant decreases in the uterine resistance but these were not dose-dependent. Acetylcholine, 5-hydroxytryptamine, noradrenaline and phenylephrine had no effect on the transuterine p.d. in vivo or in vitro or on the Isc in vitro. No significant electrical changes could be induced by adrenaline or any of the other drugs across the uteri from untreated ovariectomized rats either in vivo or in vitro. The transluminal membrane p.d. of surface endometrial cells measured with micro-electrodes was depolarized by an addition of serosal adrenaline but only 41% of the cells successfully impaled responded in this way. The results indicate that endometrial cells under oestrogen stimulation possess electrogenic processes that can be modulated specifically by adrenaline through the mediation of a serosally sited beta-adrenoceptor. The physiological role of the mechanism has yet to be established.
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PMID:Rat endometrial bioelectric activity in vivo and in vitro: effects of adrenaline. 613 98

Pharmacologic agents currently used or being studied for the treatment of schizophrenia are reviewed. Neuroleptic medications are still the mainstay of treatment, but recent studies suggest new approaches to dosage and to the treatment of acute psychosis. Lithium is beneficial in psychotic illnesses with acute onset and a remitting course, regardless of the acute psychotic symptoms. Antidepressant agents may ameliorate depression in psychotic patients, but do not improve psychotic symptoms or social withdrawal. Propranolol's reported antipsychotic action has not been confirmed by controlled studies, but the drug may have a role in treating organic psychoses. The benzodiazepines, clonidine, and carbamazepine all merit more investigation as possible treatments for psychosis. The implications of differential treatment response among schizophrenic patients are discussed.
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PMID:The pharmacologic treatment of schizophrenia: a progress report. 614 Jul 50

Propranolol (3.6 mg kg-1 day-1) was administered to guinea pigs for 14 days via subcutaneously implanted "Alzet" osmotic minipumps. Blockade of cardiac and vascular beta-adrenoceptors was confirmed by a depression of heart rate and blood pressure responses to isoprenaline in anaesthetized animals. After 14 days of propranolol treatment, minipumps were removed and 48 h later beta-adrenoceptor sensitivity was determined in cardiac and lung tissues. Left atrial inotropic responses were unaltered following propranolol withdrawal. However, right atrial chronotropic responses to sympathomimetic amines were supersensitive when compared with tissues from animals implanted with empty minipumps. Relaxation responses of lung strip preparations to beta-adrenoceptor agonists after withdrawal of propranolol were similar to controls. (3H)Dihydroalprenolol binding to ventricular and lung tissue indicated that there was no change in either the dissociation constant (KD) or the maximum number of (3H)DHA binding sites (Bm) in these tissues. These results suggest that following withdrawal from beta-adrenoceptor antagonist treatment there is a selective increase in the chronotropic sensitivity of the heart to sympathomimetic amines.
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PMID:Ex vivo examination of beta-adrenoceptor characteristics after propranolol withdrawal. 620 29

The role of the sympatho-adrenal system in the acute respiratory and cardiovascular responses to high altitude was studies in 20 volunteers during ascent to 6,000 m in a low pressure chamber, once without (control) and once with beta-adrenergic blockade. Special attention was paid to the hypoxia-induced ECG changes. Propranolol lowered the level of hypoxia-induced cardiovascular reactions, whereas it had no effect on hypoxic hyperventilation and alveolar gases. At altitude, ECG changes during myocardial depolarization occurred in both the propranolol and the control groups, probably due to the direct effects of hypoxia. During the repolarization phase, propranolol led to an almost complete abolition of S-T depression and to significant reduction of T wave flattening. The minor but still significant flattening of the T wave as well as the relative (to the heart rate) lengthening of Q-T is probably due to the direct effects of hypoxia. Propranolol abolishes or diminishes the signs of cardiac hypoxia by antagonizing the effects of catecholamine release and/or by reducing myocardial oxygen consumption, thus probable increasing the ability to withstand oxygen-want at altitude.
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PMID:Propranolol and the respiratory, circulatory, and ECG responses to high altitude. 626 74

Effort angina is the result of acute myocardial ischemia on exercise due to an imbalance between myocardial oxygen demand and supply. During exercise, ischemia is provoked by an increase in myocardial oxygen needs (tachycardia, increased blood pressure, etc.) which cannot be met by increased coronary blood flow. The commonest cause of insufficient flow is coronary atherosclerosis. Coronary spasm does, however, play a role, whether it occurs during exercise on normal or atheromatous coronary vessels. Classical anti-anginal therapy is directed towards a reduction in the intense adrenergic activity associated with exercise, and to the limitation of myocardial oxygen consumption. Calcium inhibitors which cause peripheral vasodilation, decrease ventricular wall tension and coronary resistance, are usually reserved for unstable or resistant angina. We studied 10 patients with stable effort angina for over 2 years with significant (greater than 70 per cent) atheromatous lesions on coronary angiography unsuitable for surgical treatment. The patients underwent a randomised double blind trial to compare the effects of propranolol, diltiazem and placebo. Exercise ECG was performed after a treatment period of one week, 3 hours after drug administration. The results showed a significant improvement of work capacity with propranolol and diltiazem as compared to placebo. Propranolol (160 mg/day) was more effective than diltiazem (180 mg/day) in 6 patients. In 4 cases, the improvement with diltiazem and propranolol was the same. The association of the two drugs in one open study in 5 patients was even more effective in 3 patients. The small number of patients studied makes it impossible to draw any firm conclusions. Although calcium inhibitors are the treatment of choice in coronary spasm and betablockers in effort angina, diltiazem exerts an anti-anginal effect by reduction of myocardial oxygen consumption without depression of myocardial contractility, as other workers have shown.
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PMID:[Are calcium inhibitors useful in the treatment of effort angina pectoris]. 640 53

The effects of chronic thyroxine treatment on cat soleus muscle contractions were studied. Maximum twitch tension, contraction time, half relaxation time and tension-time integral of maximal twitches of the soleus muscles of thyroxine treated cats were significantly decreased. Consequently, there was a decrease in tension and degree of fusion of incomplete tetanic contractions of the soleus muscle. The maximum tetanic tension was not statistically significantly changed, suggesting that the effects may be due to a decrease in the duration of the active state of the muscle. Isoprenaline given intravenously during incomplete tetanic contractions of the soleus muscle caused a statistically significant depression of tension in the control group but not in the thyroxine treated group. This further suggests reduction in the duration of the active state of soleus muscles of thyroxine treated cats. Propranolol injected chronically with thyroxine reversed or prevented the depression of tension caused by thyroxine treatment, suggesting the involvement of beta-adrenoceptors in these effects. The decrease in tension and degree of fusion during incomplete tetanic contractions of the thyroxine treated soleus could be responsible, at least partly, for the muscle weakness and tremor of thyrotoxicosis. Cyclic AMP may possibly be the mediator of these effects.
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PMID:Effects of thyroxine treatment on contractions of soleus muscles of anaesthetized cats. 652 66

We investigated the effect of flecainide on systolic time intervals in 6 healthy subjects. A randomized, double blind, cross-over study was designed using flecainide (2 mg/kg), propranolol (0.2 mg/kg) or saline. In comparison with placebo, flecainide increased heart rate, diastolic BP, QT-Index, QS2-Index, PEP, and reduced LVET-Index (p less than 0.05). It caused a significant increase in PR interval, QRS duration, and PEP/LVET (p less than 0.01). Propranolol, compared with placebo, decreased heart rate and systolic BP (p less than 0.05). It increased PR interval, PEP, and PEP/LVET ratio (p less than 0.05). In comparison with propranolol, flecainide increased heart rate and QRS duration (p less than 0.01, p less than 0.001 respectively). It increased diastolic BP, PR interval, QS2-Index, PEP, and PEP/LVET ratio, and decreased LVET-Index (p less than 0.05). These changes in STI induced by flecainide may be produced by depression of myocardial contractility. Intraventricular conduction delay may be an additional contributing factor.
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PMID:The effect of a new antiarrhythmic agent, flecainide acetate, on systolic time intervals. 661 15

The venous concentrations of epinephrine and norepinephrine and changes in ventilation, respiratory gases, circulation and ECG were determined in 20 young healthy male medical students during standardized stepwise ascent to 6000 m in a low pressure chamber, once without (control) and once with beta-receptor blockade (propranolol). The results show that the plasma concentration of norepinephrine increased significantly as a result of hypoxic hypoxia. The moderate increase in epinephrine was, besides the minor but significant hypoxic influence, mainly due to psychic tension. Since beta-receptor blockade does not prevent the respiratory and circulatory adjustment, beta-adrenergic stimulation is not thought to be necessary at altitude. Propranolol, on the contrary, lowers the hypoxia-induced increase in cardiac output and diminishes the ECG changes, in particular the S-T depression, significantly. By antagonizing the effects of epinephrine and by its central effects, propranolol improves subjective tolerance to altitude, and, on the other hand, by economizing the cardiac work load, the objective ability to withstand oxygen want.
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PMID:[Effect of catecholamines and propranolol on the acute acclimatization to high altitude in man]. 666 41

The central effects of propranolol, a lipophilic beta-adrenoceptor antagonist, were investigated in six healthy male volunteers using two flash fusion threshold (2FFT), simple reaction time (SRT), digital copying test (DCT), symbol digit modalities test (SDMT), Gibson spiral maze test (GSMT) and mood rating scales for tension, alertness, depression, detachment and anxiety. Compared to placebo, 2FFT was prolonged by propranolol 40, 80 and 160 mg at one or more times tested but not by propranolol 320 mg: the largest effect was seen at 3 h after 40 mg, and the effects of 40, 80 and 160 mg were significantly greater than 320 mg at 2 h. SRTs were significantly prolonged by all doses of propranolol at 2 and 3 h and by 40 and 80 mg doses at 5 h. DCT was lowered by 40 and 80 mg at 2 and 3 h by 80 mg at 5 h, and by 320 mg at 2 h, but the 160 mg dose had no effect. Propranolol impaired the expected retest gain of the SDMT with all doses except 320 mg and at 2 h after 40, 80 and 160 mg, performance was actually worsened. Mood rating scales showed increased detachment with 40 mg and decreased alertness with 80 and 320 mg. The results show that propranolol has central effects in man: the effects appeared to be greater with lower doses, 40 and 80 mg, than with higher doses, 160 and 320 mg.
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PMID:Central effects of single oral doses of propranolol in man. 669 87


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