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)

Dietary measures have achieved mixed results in the management of liver disorders. Although a high energy diet may shorten the course of viral hepatitis by a relatively small amount, dietary restriction is usually of no benefit in compensated cirrhosis. Restriction of sodium intake to 22 to 60 mol/day leads to resolution of cirrhotic ascites in approximately 20% of patients, and reduces the requirement for diuretics in the remainder. In advanced liver disease, diet plays an important role in the avoidance of portal-systemic encephalopathy (PSE), with the tolerance of most nutrients, most importantly protein, being sharply reduced. Despite the frequent presence of carbohydrate intolerance in liver disease, carbohydrate supplementation may be required to ensure adequate utilisation of the reduced dietary protein intake. Zinc supplementation may also be required in liver cirrhosis to compensate for a deficiency. Bed rest is an important component of the management of acute and chronic liver disorders, together with the avoidance of fatigue. Abstinence from alcohol is required in alcoholic liver disease patients, who should receive parenteral thiamine 100 mg and other vitamin and mineral supplementation as required. Agents acting on the ascending loop of Henle [such as furosemide (frusemide)] or the distal tubule (such as spironolactone) are the diuretics most frequently employed to mobilise ascites in cirrhosis, the latter drug being the more effective in nonazotaemic patients. In the absence of oedema, the diuresis should be restricted to a maximum of 750 ml/day; however, patients with oedema may safely undergo a diuresis of less than or equal to 1.5 L/day. Diuretic therapy is often associated with renal complications, such as azotaemia (usually reversible) and severe hyponatraemia in cirrhotic patients with ascites; spironolactone may produce antiandrogenic adverse effects. Lactulose, used in the treatment of acute and chronic PSE, acts by inhibiting gastrointestinal absorption of ammonia and other toxic nitrogenous substances, and by reducing urea degradation. Other pharmacological treatments, such as branched-chain amino acids and benzodiazepine antagonists have a limited role in the management of PSE. Chronic cholestasis has been treated with cholestyramine and fat-soluble vitamins, whereas ursodeoxycholic acid appears to be a promising agent in the treatment of primary biliary cirrhosis. In chronic hepatitis, the prevention of development of cirrhosis is a primary treatment goal which has been attempted with variable success using antifibrotic drugs such as penicillamine and colchicine.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Traditional management of liver disorders. 208 80

Five patients with McArdle's disease entered a double-blind, placebo-controlled, cross-over study of dantrolene sodium. None of the patients experienced beneficial effect of dantrolene sodium medication. Each patient performed 2 exercise tests. Surface EMG during exercise tests without medication showed a temporary increase in EMG activity during the adaptation phase. Quite unexpectedly however, in view of the negative clinical results, this electrophysiological manifestation of muscle fatigue during the adaptation phase diminished or disappeared in all patients investigated when dantrolene sodium was used.
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PMID:Dantrolene sodium does influence the second-wind phenomenon in McArdle's disease. Electrophysiological evidence during exercise in a double-blind placebo-controlled, cross-over study in 5 patients. 208 28

Within the framework of an open, multicenter study of 16 physicians treated 206 hypertensive patients with a daily dose of 2 x 30 mg to 2 x 90 mg of urapidil over a period of 3 years. Data are available on 182 patients for the entire study period. 24 patients discontinued the study due to adverse effects (n = 2), an inadequate effect (n = 2), or for reasons unrelated to therapy (n = 20); 58 (28.2%) patients had complaints. The most frequently reported symptoms were nausea, dizziness, drowsiness and fatigue. No relevant changes in laboratory values were observed. Average body weight remained constant and there were no signs of sodium or water retention. In the first year systolic blood pressure was reduced by 25 mm Hg from 174 +/- 13 mm Hg to 149 +/- 10 mm Hg (mean value +/- SD), and diastolic pressure by 17 mm Hg from 103 +/- 6 mm Hg to 86 +/- 6 mm Hg. At the same average dose this drop in BP persisted in the second year (150 +/- 12/86 +/- 7 mm Hg) and the third year (146 +/- 10/85 +/- 7 mm Hg), indicating that there was no decrease in urapidil effect. The pulse rate fell from 77 +/- 8 beats/minute to 74 +/- 6 beats/minute and remained virtually constant over the next 2 years.
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PMID:[Long-term antihypertensive therapy with urapidil. A 3-year open, multicenter trial of tolerance, safety and effectiveness]. 211 78

Twenty-two Standardbred horses in race training were used in a crossover experiment to determine the effect of oral sodium bicarbonate (NaHCO3) administration on performance and metabolic responses to a 1.6-km (1-mile) race. Horses were paired and one horse in each pair was treated with either NaHCO3 (300 mg/kg BW) or a placebo, 2.5 h before they raced against each other. Each horse was scheduled to compete in two races, approximately 1 wk apart, one on each treatment. Horses always raced in the same pairs. Fourteen horses successfully completed both races. Jugular blood samples were obtained 1.5 h after treatment (rest), immediately before racing, 5 min post-race and 15 min post-race. In six horses, blood samples also were obtained 30 min post-race. Race times averaged 1.1 s faster after NaHCO3 treatment (P less than .1). Sodium bicarbonate treatment also elevated blood pH (P less than .05). In the horses sampled 15 and 30 min post-race, blood lactate disappearance was faster with the NaHCO3 treatment (P less than .05). The NaHCO3 may delay the fatigue precipitated by i.m. acidosis. Because other factors may limit performance (musculoskeletal soundness, cardiovascular and respiratory ability), NaHCO3 would not be expected to enhance the performance of all horses. However, the effect of NaHCO3 on lactate clearance may have implications for all intensively worked horses; because lactate and the associated hydrogen ions are believed to cause muscle damage and soreness, any mechanism to increase their removal rate could benefit the equine athlete.
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PMID:Effect of sodium bicarbonate on racing Standardbreds. 215 89

Maintenance of low coronary flow (1 ml/min) during 40 or 70 min of anoxia maintained function and prevented Ca2+ overload during reoxygenation in isolated rat hearts. In comparison, recovery from 40 min of global ischemia resulted in only 20% of preischemic function and an increase in end-diastolic pressure (LVEDP) to 39 mmHg. Reperfusion Ca2+ uptake rose from 0.6 to 10.2 mumol/g dry tissue. Intracellular Na+ (Nai+) increased from 13 to 61 mumol/g dry tissue after 40 min of global ischemia, but was unchanged in hearts with low flow anoxia. When glucose and pyruvate were omitted from buffer used for anoxic perfusion, recovery was only 15% of preanoxic values, LVEDP rose to 32 mmHg, and reperfusion Ca2+ uptake was 7.2 mumol/g dry. In addition, Nai+ increased (47.4 mumol/g dry tissue) and ATP was depleted (1.0 mumol/g dry tissue) in the absence of substrate. In anoxic hearts supplied substrate, Nai+ stayed low (12 mumol/g dry tissue) and ATP was preserved (11.6 mumol/g dry tissue). Addition of ouabain (100 or 200 microM) and provision of zero-K+ buffer increased Nai+ and resulted in impaired functional recovery, increased LVEDP, and greater reperfusion Ca2+ uptake. These interventions also decreased energy availability in anoxic hearts. To distinguish between effects of Na+ accumulation and ATP depletion, monensin, a Na+ ionophore, was added during low flow anoxia. Monensin increased Nai+, decreased functional recovery and increased reperfusion Ca2+ uptake in a dose-dependent manner (1-10 microM) without changing ATP content. These results suggested that reduction of Nai+ accumulation by maintenance of Na+, K+ pump activity was the major mechanism of the beneficial effects of low coronary flow on reperfusion injury.
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PMID:Na+ accumulation increases Ca2+ overload and impairs function in anoxic rat heart. 215 54

The Na-K-ATPase is the enzymatic basis of a energy-dependent transport of sodium and potassium through the cell membrane and is therefore of importance to the survival of organs during periods of decreased energy supply. In the present paper the influence of various preservation solutions on the activity of this enzyme was examined. It was shown that Na-K-ATPase activity in rat kidneys did remain unchanged after 48 hour preservation in various preservation solutions (Bretschneider, Ross, Collins, Sacks, Belzer). Therefore, its estimation is no valuable for evaluation of preservation solutions.
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PMID:[Na K ATPase activity in rat kidneys following storage at 4 degrees C in various kidney preservative solutions]. 216 14

We report a case of 47-year-old woman with an isolated deficiency of adrenocorticotropic hormone. She was admitted complaining of fatigue and frequent loss of consciousness. The patient developed severe hyponatremia (100 mEq/l) after five days of the admission. Her plasma renin activity and plasma aldosterone concentration were low though she was dehydrated. After the treatment of dehydration, plasma osmolality was low but high plasma antidiuretic hormone (ADH) level sustained. Both high urinary sodium excretion and low urinary aldosterone excretion still remained after one month of replacement therapy with prednisolone. But, glomerular filtration rate and a response of urinary volume to acute water loading were normalized. These results suggested that severe hyponatremia of the patient was caused by an inappropriate secretion of ADH and suppression of renin-aldosterone system. We consider the suppression of renin-aldosterone system was partially independent of an inappropriate secretion of ADH.
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PMID:[Hyponatremia in isolated deficiency of adrenocorticotropic hormone: role of a decrease in aldosterone secretion independent of antidiuretic hormone excess]. 217 15

The purpose of these experiments was to examine the influence of various fluid replacement drinks on exercise-induced disturbances in homeostasis during heavy exercise. Nine trained cyclists performed constant load exercise on a cycle ergometer to fatigue on three occasions with 1-week separating experiments. The work rate was set initially at approximately 85% of VO2max (range 82-88%) with fatigue being defined as a 10% decline in power output below the initial value. During each experiment subjects consumed one of the following three beverages prior to and every 15 min during exercise: (1) non-electrolyte placebo (NEP; 31 mosmol.kg-1); (2) glucose polymer drink containing electrolytes (GP; 7% CHO, 231 mosmol.kg-1), and (3) electrolyte placebo drink without carbohydrate (EP; 48 mosmol.kg-1). Both the GP and EP beverage contained sodium citrate/citric acid (C) as a flavoring agent while C was not contained in the NEP drink. Although seven of nine subjects worked longer during the GP and EP treatment when compared with the NEP trial, the difference was not significant (P greater than 0.05). No differences (P greater than 0.05) existed between the GP and EP treatments in performance time. Exercise changes in rectal temperature, heart rate, delta % plasma volume and plasma concentrations of total protein, free fatty acids, glucose, lactate, potassium, chloride, calcium, and sodium did not differ (P greater than 0.05) between trials.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fluid replacement drinks during high intensity exercise: effects on minimizing exercise-induced disturbances in homeostasis. 231 95

Our understanding of the time course of recovery from exertional heatstroke (EH) and the heat acclimation ability of prior EH patients is limited. This manuscript reviews previous findings regarding recovery from EH and presents original research involving the heat acclimation ability of 10 prior EH patients (PH) and 5 control subjects. Heat acclimation, by definition, distinguishes heat-intolerant from heat-tolerant prior heatstroke patients. Nine PH exhibited normal heat acclimation adaptations (40.1 degrees C, 7 d, 90 min.d-1), thermoregulation, sweat gland function, whole-body sodium and potassium balance, and blood values at 61 +/- 7 d after EH. One PH (subject A) did not adapt to exercise in the heat, was defined heat intolerant, but subsequently was declared heat tolerant (11.5 months post-EH). Three PH exhibited large, unexpected increases in serum CPK levels, which resolved upon subsequent testing, and were probably related to their detrained state and the exercise which they performed. It was concluded that: 1) sleep loss and generalized fatigue were the most common predisposing factors for PH; 2) recovery from EH was idiosyncratic and may require up to 1 year in severe cases; 3) PH were not hereditarily heat intolerant, prior to EH; 4) no measured variable predicted recovery from EH, or heat acclimation responses; 5) heat intolerance occurs in a small percentage of prior heatstroke patients, and may be transient or persistent.
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PMID:Time course of recovery and heat acclimation ability of prior exertional heatstroke patients. 240 45

Fatigue from high frequency stimulation is associated with EMG signal changes, which are primarily due to a slowing of the sarcolemma conduction velocity. In the present study, in which isolated mouse soleus and extensor digitorum longus muscles have been studied, it is shown that the action potential propagation velocity is (1) decreased by an increased extracellular potassium concentration, (2) independent of extracellular pH, (3) decreased by low intracellular pH, and (4) nearly independent of moderate changes in the sodium gradient. The EDL muscle is more affected than the soleus muscle. The ion effects on propagation velocity are seen within the physiological ranges. The propagation velocity was decreased after 2 min of electrical stimulation and recovered with a time course similar to the pH recovery. The effects of extracellular potassium and internal pH are due to independent mechanisms.
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PMID:Muscle action potential propagation velocity changes during activity. 245 55


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