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)

The effect of pretreatment for 3 weeks with propranolol 20 mg/kg/day on cardiovascular function during increasing depths of halothane anaesthesia (range 1.0-2.5% inspired halothane with IPPV and normocapnia) were studied in a group of seven closed-chest dogs which had been implanted previously with cardiovascular flow- and pressure-measuring instruments. The results were compared with those observed in a similar group of five untreated dogs. Propranolol pretreatment resulted in a small degree of additional cardiac depression at any inspired halothane concentration. The cardiac depressant effects of propranolol and halothane were found to be simply additive and therefore predictable. The presence of propranolol did not result in morbidity or mortality at any depth of halothane anaesthesia.
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PMID:Haemodynamic interactions of high-dose propranolol pretreatment and anaesthesia in the dog. I: Halothane dose-response studies. 127 98

After chronic administration of propranolol (1 and 5 mg/kg, 14 days) to rats time-course of forced swimming changed with the decrease of rhythmical index of depression. The drug attenuated depressogenic properties of reserpine and clonidine. Propranolol antidepressive activity is attributed to blockade cerebral adrenoreceptors.
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PMID:[The antidepressive properties of anaprilin]. 128 90

The effects of halothane on the effective refractory period (ERP) and the ventricular activation were examined in a canine myocardial infarction model, and compared with those of propranolol. Halothane reduced the heart rate and prolonged the ERP in both normal and infarcted zones. A prolongation of ERP with halothane was also observed during atrial pacing at the same rate as in control, but the effect was less than during sinus rhythm. Halothane (1 MAC) further delayed or blocked the delayed activation in the infarcted zones with only slight effects on the activation of the normal zones. Propranolol (0.2 mg/kg) prolonged ERP during sinus rhythm, but it did not affect either the ERP or ventricular activation during atrial pacing. In conclusion, halothane produced a selective depression of the delayed activation and the prolongation of ERP, which may be caused by both direct effects on the myocardium and secondary effects such as a reduction of the heart rate. These effects of halothane may contribute to its antiarrhythmic effects in the myocardial infarction model which have been previously reported.
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PMID:Comparison of the effects of halothane and propranolol on the effective refractory period and the ventricular activation in a canine myocardial infarction model. 128 97

Examination of central hemodynamics in patients in the preperfusion period of radical correction of Fallot's tetrad has demonstrated that after pericardiotomy and the onset of surgical manipulation on the heart there was a depression of circulation both during the use of intravenous total anesthesia on the basis of ketamine and ataralgesia. The depression was more manifest under ataralgesia. The depression of circulation was paralleled by the deepening of initial hypoxemia. Analysis of the efficacy of medicamentous agents with regard to the specific features of intracardiac anatomy of the outlet of the right ventricle, estimated intraoperatively, has established that administration of phenylephrine at a rate of 3 micrograms/kg favoured an increase of partial oxygen pressure and arterial blood saturation with hemoglobin whatever the anatomo-morphological type of stenosis of the outlet of the right ventricle. Propranolol promoted the improvement of arterial blood oxygenation but in the muscular type stenosis of the outlet of the right ventricle. Meanwhile the use of the drugs possessing a beta-adreno-stimulating effect brought about the deepening of hypoxemia.
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PMID:[Approaches to prevention and treatment of arterial hypoxemia in the pre-perfusion period of radical correction of Fallot's tetrad]. 138 54

Paroxysmal supraventricular tachycardia is the most common sustained cardiac arrhythmia in pregnant women. Because nearly 50% of these supraventricular tachyarrhythmias fail to respond to vagal maneuvers, other therapies are used, including electrocardioversion and pharmacologic agents. Propranolol, verapamil, and adenosine have Food and Drug Administration-approved labeling for acute termination of supraventricular tachycardia. Verapamil has been the most commonly used agent in the general population but it has several shortcomings, such as its potential to cause or exacerbate systemic hypotension, congestive heart failure, bradyarrhythmias, and ventricular fibrillation. In addition, verapamil readily crosses the placenta and has been shown to cause fetal bradycardia, heart block, depression of contractility, and hypotension. Adenosine has several advantages over verapamil, including rapid onset, brevity of side effects, theoretical safety, and probable lack of placental transfer. Adenosine ultimately may prove to be the preferred agent for termination of paroxysmal supraventricular tachycardia in the gravid woman.
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PMID:Adenosine in the treatment of maternal paroxysmal supraventricular tachycardia. 149 12

We studied the short-term effects of oral administration of nisoldipine (10 mg) and propranolol (80 mg) alone and in combination in 14 patients with chronic exertional angina pectoris in a double-blind, randomized, cross-over study. The 14 patients (13 men and 1 woman, mean age 56 +/- 7 years) performed symptoms-limited bicycle exercise stress test 3 h after placebo or active substance administration. Maximal work load, exercise duration, and time to 1-mm ST segment depression were significantly increased and ST depression at peak exercise was significantly decreased by drugs alone and in combination. Propranolol and nisoldipine alone improved exercise duration similarly and as well as the combination; however, a different response to the three pharmacologic interventions was found in patients treated with single drugs. The improvement in exercise tolerance was associated with rate-pressure product values at peak exercise, unchanged after nisoldipine and significantly reduced after both propranolol alone and in combination. After placebo, all patients had exercise-induced angina, in 9, 8, and 4 patients after nisoldipine, propranolol, and the combination of the two drugs, respectively. Nisoldipine is effective in the treatment of effort angina and its combination with propranolol may be useful and superior in patients who show poor response to monotherapy.
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PMID:Acute effects of nisoldipine, propranolol, and their combination in patients with chronic stable angina: a double-blind, randomized, cross-over, placebo-controlled study. 169 90

Effects of 1% anaprilin instillations on intraocular pressure, ocular hydro- and hemodynamics, anterior chamber depth, pupil width, ocular functions, systemic arterial pressure and pulse rate were studied in 57 patients (94 eyes) with primary open-angle glaucoma. Anaprilin has shown a manifest hypotensive effect, explained by depression of aqueous humor production. The drug did not influence the visual functions, pupil width, or anterior chamber depth. A synergic effect on intraocular pressure was observed when anaprilin was combined with pilocarpine or clopheline.
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PMID:[Effectiveness of anaprilin in the treatment of glaucoma]. 203 14

There is circumstantial evidence that increases in prolactin secretion evoked by L-tryptophan infusion involve 5-HT1 receptors, whereas growth hormone responses do not. Propranolol is a beta-adrenoceptor antagonist that also possesses antagonist properties at 5-HT1 receptors. Propranolol (80 mg, PO) failed to attenuate the prolactin response to L-tryptophan infusion (100 mg/kg, IV) in seven volunteers; the role of 5-HT1 receptors in this response remains uncertain. The growth hormone response to tryptophan was enhanced by propranolol, consistent with previous reports of an inhibitory beta-adrenoceptor influence on GH secretion. Excessive beta-adrenoceptor function might explain the blunted growth hormone response to tryptophan in depression.
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PMID:Hormonal response to L-tryptophan infusion: effect of propranolol. 208 37

Long-acting Propranolol (160 mg/day) and Amiodarone (200 mg/day after impregnation) were compared in chronic stable angina pectoris. Forty-three patients with stable angina of effort were included in a randomised double blind trial (19 in the amiodarone and 24 in the propranolol group). The duration of the study was 8 weeks; the placebo phase (2 weeks) was followed by 6 weeks of active treatment. An exercise stress test was performed before and after the treatment period. The number of episodes of angina and the consumption of glyceryl trinitrate decreased significantly (p less than 0.001) in the same proportion with both drugs with respect to the placebo period. The time to the appearance of criteria of positivity of the exercise stress test increased from 6.82 +/- 0.50 mn to 8.35 +/- 0.50 mn with amiodarone, and from 7.15 +/- 0.47 mn to 9.50 +/- 0.52 with the propranolol preparation. This improvement was very significant compared with the placebo phase (p less than 0.001) but the difference between the two drugs was not statistically significant (p = 0.39). The other parameters which were studied (time to onset of angina, total duration of exercise, maximum heart rate, double product, maximum ST depression) changed in a parallel fashion significantly versus placebo. There were no differences between the two treatment groups with the exception of the resting heart rate which decreased more in patients on propranolol (80.94 +/- 3.92 to 62.47 +/- 1.97) than in patients on amiodarone (84.87 +/- 2.63 to 73.41 +/- 2.01; p less than 0.0005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anti-angina effect of amiodarone versus delayed-action propranolol. A double-blind randomized study]. 212 69

The relationship between propranolol and depression is a subject of controversy. Numerous case reports suggest that propranolol can cause depression, but two small prospective trials have failed to confirm this. The contemporary psychiatric literature is divided as to whether propranolol can cause depression. This study addresses this issue by re-analyzing side effect data from clinical trials of propranolol as an antihypertensive agent. A literature review was carried out and the data were analyzed using meta-analytic statistical techniques. Propranolol was found to cause depression as a side effect with a statistically greater frequency than the control medications used in these trials. As other side effects of propranolol include fatigue, diminished energy, decreased libido, anorexia and poor concentration, it is suggested that propranolol is a cause of organic mood disorder, depressed type.
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PMID:Propranolol and depression: evidence from the antihypertensive trials. 214 Feb 88


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