Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some of the symptoms and signs of hypothyroidism and hyperthyroidism in elderly patients may be mistakenly attributed to "old age." Weight loss, muscle weakness, tremor, angina, congestive heart failure--all signs of hyperthyroidism--are also concomitants of aging. Fatigue, sluggishness, withdrawal behavior, senile atrophic skin changes--all signs of hypothroidism--are also a part of the normal aging process. Although screening elderly people for thyroid disease is economically unsound, the physician should maintain a high index of suspicion of its presence. Laboratory tests must be interpreted with extra care. Values of 131I uptake, serum T4 and T3, thyroid-stimulating hormone, and thyrotropin-releasing hormone are all helpful in diagnosis. Thyroid disease is easily treated in elderly patients, and results often are dramatic. Propranolol is effective in thyrotoxic patients when symptoms require prompt relief. The definitive treatment, however, is 131I; antithyroid drugs are difficult to manage. Hypothyroidism is easily treated with T4.
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PMID:How thyroid disease presents in the elderly. 2 76

Isolated dog hearts perfused with blood from a donor dogand driven at two heart rates were used to compare the effects of propranolol with those of its quaternary ammonium derivative on atrial, atrioventricular (AV) nodal, and His-Purkinje conduction. Propranolol slowed only AV-nodal conduction, increasing the minimal conduction time and the effect of prematurity, without affecting fatigue. Practolol did not have this effect. Dimethylpropranolol had similar but not identical effects on the AV node, but also slowed atrial and ventricular conduction. In contrast with the quaternary derivative of lidocaine, dimethylpropranolol's effect on atrial and ventricular conduction was not dependent on the heart rate. The effect of dimethylpropranolol on ventricular conduction was observed at doses lower than those reported by others to be antiarrhythmic.
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PMID:The effect of propranolol and dimethylpropranolol on cardiac conduction. 48 71

The effects of propranolol on electrical and mechanical activity during tetanic stimulation of the diaphragm and leg muscles, and on the heart rate, were studied in the anaesthetized rabbit. Propranolol (from 0.5 mg/kg) reduced the EMG evoked in diaphragm by phrenic nerve stimulation (50/sec) and the EMG and force of contraction during periods of increased respiratory drive obtained by partial tracheal obstruction. The heart rate was lowered by 10-25%. In the indirectly or directly stimulated leg muscles, the drug induced high frequency inhibition of EMG and tetanic contractions (100/sec) without affecting twitch contractions. The inhibitory effect of propranolol on skeletal muscle was probably not caused by beta-adrenergic block, but by stabilization of the sarcolemma. The results suggest that the high frequency inhibitory effect might contribute to the fatigue and reduced work capacity frequently observed when high doses of propranolol are given to man and animals.
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PMID:Inhibitory effect of propranolol on tetanic contraction in rabbit. 85 4

The electrophysiologic effects of intravenously administered propranolol (0.1 mg/kg) on three parameters of sinus node function were examined in ten symptomatic patients with sinus node dysfunction. The patients ranged in age from 26 to 79 years. Symptoms ranged from fatigue to frank syncope. Sinoatrial (SA) block and sinus pauses were observed in one patient; sinus pauses alone were observed in three patients. Five (5/10) patients had intraatrial block; three (3/10) patients had atrioventricular block; four (4/10) patients had an intraventricular conduction disturbance. At the time of electrophysiologic study, two patients had a control spontaneous sinus cycle length that exceeded 1000 msec. Following propranolol, the mean spontaneous cycle length increased by 17.4% (924 to 1085 msec, P less than 0.005) and spontaneous second degree SA block reappeared in the one patient. The maximum escape cycle ranged from 116% to 229% of the prepacing spontaneous cycle length and was considered to be prolonged in two of ten patients. Propranolol had no significant effect on the maximum escape cycle/prepacing cycle length X 100 (%). The estimated sinoatrial conduction time (SACT) was determined in seven patients and ranged in value from 120 to 238 mes. Propranolol increased the mean value of the estimated SACT from 179 to 213 msec, P less than 0.025. Propranolol may cause marked bradyarrhythmias in some patients with sinus node dysfunction, and should be used with caution in these patients.
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PMID:Electrophysiologic effects of propranolol on sinus node function in patients with sinus node dysfunction. 94 74

1. The differential effects of beta-adrenoceptor subtypes on potassium fluxes and exercise capacity were compared in eight healthy young men using single oral doses of the selective beta 2-adrenoceptor antagonist ICI-118551, the selective beta 1-adrenoceptor antagonist atenolol or the non-selective beta-adrenoceptor antagonist propranolol. The study was randomized, double-blind and placebo controlled. 2. Potassium in the venous effluent from the exercising muscles increased progressively with increasing exercise intensity. This response was augmented by propranolol, whereas neither atenolol nor ICI-118551 modified the response. After exercise potassium concentration fell exponentially with no difference between the treatment regimens. 3. Cumulative work was significantly reduced by ICI-118551 (6.4%, P = 0.04) and by propranolol (12.4%, P less than 0.01), whereas the reduction with atenolol (5.6%) did not reach statistical significance. 4. Atenolol and propranolol reduced peak heart rate by 23% and 29%, and peak systolic blood pressure by 9% and 11% respectively during maximal exercise. ICI-118551 caused a non-significant reduction in heart rate during submaximal exercise, with a significant reduction at maximum exercise (6% reduction), whereas systolic blood pressure was not different from placebo. Diastolic blood pressures were similar across all treatment regimens. 5. Similar glucose concentrations were obtained at baseline and at exhaustion during all treatment regimens. Lactate concentrations were comparable for any given exercise intensity irrespective of treatment regimens. Propranolol reduced lactate concentrations from the exercising muscles at maximum exercise in proportion to the reduction of maximal exercise capacity. 6. The subjective perception of fatigue was not affected by either beta 1- or beta 2-adrenoceptor blockade.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of selective beta 2-adrenoceptor blockade on serum potassium and exercise performance in normal men. 168 47

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

The clinical efficacy of flunarizine and propranolol for the prevention of migraine attacks was assessed in 33 children in a double blind study. After a run-in phase of one month, 32 patients started the active medication. A reduction in the number of migraine attacks was observed in 75% of the flunarizine group and in 73.8% of the propranolol group. Propranolol also reduced the severity of attacks. Transient side effects were observed in 3 of 17 of the flunarizine group and in 5 of 15 of the propranolol group. The most frequent side effect was increased fatigue, which required interruption of therapy in 2 patients of the propranolol group.
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PMID:[The treatment of juvenile migraine using flunarizine or propranolol]. 225 92

We report on the distress associated with physical symptoms in 761 male hypertensive patients enrolled in a clinical trial of the effects of captopril, methyldopa or propranolol on quality of life. Educational level at entry into the trial showed a negative association with a series of physical symptom distress items among patients not previously treated with antihypertensive medications but no association with symptoms among the previously treated. Over the 24 weeks of therapy captopril as monotherapy was associated with no change from baseline in distress in all symptoms examined. In contrast, distress increased in the methyldopa treated patients for dry mouth and blurred vision. Propranolol treated patients had increased "trouble getting breath," bradycardia, shortness of breath or wheezing, and blurred vision. Between group comparisons revealed significant differences favorably comparing captopril to both methyldopa and propranolol in regard to fatigue, and blurred vision, as well as to methyldopa alone for dry mouth and "feeling worn out." There were significant differences as well between captopril and propranolol with patients on propranolol worsening in bradycardia. Other comparisons of patients on propranolol and methyldopa monotherapy showed propranolol patients worsening in bradycardia and loss of taste, but methyldopa patients reported more dry mouth and feeling worn out than those on propranolol. The addition of hydrochlorothiazide to therapy worsened total physical symptom distress scores for methyldopa and propranolol patients. This study confirms the value of methods which assess the degree of distress associated with symptoms commonly reported by hypertensive patients receiving antihypertensive medications. This approach can be useful in establishing a treatment regimen least likely to cause distress and can be of value in preserving quality of life, preventing noncompliance, and withdrawal from treatment.
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PMID:Self-reported side effects from antihypertensive drugs. A clinical trial. Quality of Life Research Group. 240 65

The interaction between oral verapamil and propranolol may involve negative chronotropic, inotropic or dromotropic effects. The immediate effects of orally administered verapamil (120 mg) and propranolol (80 mg), alone and combined, on submaximal exercise hemodynamics and on pharmacokinetics were studied in eight healthy male volunteers in a randomized, double-blind, crossover manner. Maximum effects on heart rate, systolic blood pressure, PR interval and rate-adjusted PR prolongation were greatest with the combined administration of verapamil and propranolol. The combination caused a high frequency of adverse drug events, predominantly exercise fatigue. Verapamil increased the AUC and Cmax and shortened the tmax of propranolol. Propranolol decreased the AUC and Cmax of verapamil. The greater reduction of heart rate with the combination of verapamil and propranolol was only partially explained by higher plasma concentrations of propranolol. The combination of propranolol and verapamil produced clinically important synergistic adverse effects during exercise. Negative dromotropic effects occurred primarily by direct AV node inhibition and were more important than previously recognized.
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PMID:Synergistic adverse hemodynamic interaction between oral verapamil and propranolol. 279 49

To investigate adrenergic receptor-mediated responses in dog gastrocnemius-plantaris muscle, several catecholamine agonists, isoproterenol, epinephrine, norepinephrine, and phenylephrine, and two antagonists, propranolol and phenoxybenzamine, were given during repetitive, isotonic, tetanic contractions. The response variables that were measured were muscle blood flow, shortening during constant load contractions, and arterial and venous O2 and lactate concentrations. The calculated variables were O2 uptake (VO2), net lactic acid output (L), and power output. In the control experiments, the contractions increased VO2 to approximately 50 times rest by 2 min. Thereafter, shortening, work, and VO2 declined together by 17% at 30 min, indicating muscle fatigue. L increased rapidly to nearly 0.8 mumol X g-1 X min-1 by 2 min, declined to 0.3-0.4 mumol X g-1 X min-1 by 7 min, and was like rest at 15, 22.5, and 30 min. The arterial lactate concentration rose steadily from rest to 30 min of contractions. Epinephrine infusion stopped the decline of VO2 during the contractions, but this effect was not observed with the other agonists. Propranolol decreased VO2 compared with controls at 22.5 and 30 min of contractions. Phenoxybenzamine decreased VO2 compared with controls at all times during contraction, and the decline with time was present. Coinfusion of epinephrine with propranolol reduced the decline in VO2 observed with propranolol alone. Both epinephrine and isoproterenol increased L compared with controls. This epinephrine response was antagonized by propranolol but enhanced by phenoxybenzamine. Both isoproterenol and epinephrine infusions increased arterial lactate concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of adrenergic agonists and antagonists on muscle O2 uptake and lactate metabolism. 288 2


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