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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cardiocirculatory actions on the oral vasodilator prazosin were evaluated by cardiac catheterization, forearm plethysmography, echocardiography, treadmill exercise and symptoms in patients with advanced long-standing congestive heart failure. The administration of oral prazosin (2 to 7 mg) reduced forearm venous tone and forearm vascular resistance. Concomitantly, mean systemic arterial pressure and left ventricular filling pressure decreased, and the cardiac index increased. These effects of a single dose of prazosin on left ventricular function were rapid in onset, maximal at 1 hour and sustained for the entire 6-hour period of observation. After two weeks of outpatient therapy with 2 to 7 mg of prazosin four times daily, echographic end-diastolic dimension decreased, whereas the duration of treadmill exercise increased. Symptoms (dyspnea, fatigue, angina) were diminished throughout the course of prazosin therapy, and there was an improvement in the New York Heart Association functional class from 3.7 to 2.2. Thus, prazosin possesses sustained nitroprusside-like balanced dilator actions of the systemic arterial and venous beds, which are effectively translated into the beneficial hemodynamic effects of augmenting cardiac output and relieving excessive left ventricular end-diastolic pressure. The delayed vasodilator tolerance that occurs in 30 percent of the patients is prevented by the prior use of aldosterone antagonists and is easily treated when present. Subacute hemodynamic suppression of beneficial prazosin vasodilator actions is transient and does not preclude successful sustained prazosin therapy of severe heart failure.
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PMID:Therapeutic application of prazosin in chronic refractory congestive heart failure. Tolerance and "tachyphylaxis" in perspective. 724 73

Primary adrenal insufficiency is characterized by cortisol and aldosterone deficiency; in the secondary form, cortisol alone is decreased. The symptoms are usually nonspecific and include hypotension, weight loss, and fatigue; volume depletion, hyperkalemia, and hyperpigmentation may be present in the primary form but are uncommon in the secondary form. The most common cause of secondary adrenal insufficiency is steroid therapy, which produces adrenal suppression in relation to the dose and duration of use. Sudden withdrawal may precipitate adrenal crisis; therapy must be continued until adrenocortical function recovers. Because cortisol deficiency increases vulnerability to stress, patients with known or suspected adrenal insufficiency require glucocorticoid prophylaxis before any surgical procedure, major or minor. Hydrocortisone, not cortisone acetate, should be used.
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PMID:Preventing adrenal insufficiency during surgery. 737 7

A twenty-one-year-old male was admitted to our hospital because of hypertension and proteinuria. He had felt general fatigue and low grade fever for one month. Blood pressure was 180/120 mmHg on admission. Laboratory findings showed 3+ proteinuria and 1+ occult blood in urinalysis; an accelerated erythrocyte sedimentation rate (ESR) of 39 mm/hr; elevation of LDH to 755 IU/l. Antinuclear antibody was positive with a titer of 1: 160, with a speckled pattern. Plasma renin activity and serum aldosterone were markedly elevated to 25.8 ng/ml/hr and 585.3 pg/ml, respectively. Renal function had declined mildly; endogenous creatinine clearance was 60 ml/min. Renal arteriogram demonstrated multiple intrarenal aneurysms in the bilateral kidneys. Aneurysms, 5-8 mm in diameter were located in the arteries from the interlobar to interlobular region. He was diagnosed as having polyarteritis nodosa (PN) and was then treated with 20 mg/day of prednisolone and monthly pulse therapy of cyclophosphamide. After steroid, cyclophosphamide and anti-hypertensive therapy, he became well and had normal blood pressure. The patient was considered a rare case of PN with multiple intrarenal aneurysms and accelerated hypertension. We discuss aneurysms in PN and accelerated or malignant hypertension documented in the literature.
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PMID:[A case of polyarteritis nodosa presenting with multiple intrarenal aneurysms and accelerated hypertension]. 769 55

It is traditionally considered that angiotensin--converting enzyme inhibitor (ACEI) and spironolactone could not be used simultaneously because of the assumed risk of hyperkalemia. However, despite ACEI therapy edema and congestive status remain in some of the patients with severe congestive heart failure (CHF). In order to seek an effective therapy for these patients, we observed the efficacy and safety of captopil plus spironolactone in patients with refractory CHF, with strict monitoring of renal function, serum and urine electrolytes and blood pressure (BP). Thirty-five patients with refractory CHF and New York Heart Association functional class IV without renal dysfunction, hypotension and hyperkalemia, whose plasma aldosterone (ALD) level in 88.6% of them was above normal value, were randomly assigned to group A (n = 16, captopril alone) and B (n = 19, captopril plus spironolactone) for a 4-week treatment. The dosage of both drugs was individually adjusted in time according to the results of serum potassium and renal function. The improvement in dyspnea--fatigue ratings, urinary volume and Na+/K+ ratio in group B was more significant than that in group A, and the plasma ALD level in group B decreased obviously while it remained high in group A after therapy. Two patients in group B who had had normal plasma ALD level with urinary Na+/K+ ratio > 1.0 before the therapy did not exhibit any clinical improvement. A strong negative correlation was found between plasma ALD level and urinary Na+/K+ ratio (correlation coefficient -0.689, P < 0.01). None of the patients had obvious hyperkalemia and hypoaldosteronism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Combined therapy of captopril and spironolactone for refractory congestive heart failure. 780 62

The effect of carmoxirole, a presynaptic dopamine (DA2) receptor agonist, on blood pressure, plasma catecholamines, renin-aldosterone and atrial natriuretic peptide and the intracellular concentration and transmembrane fluxes of Na+ and K+, in erythrocytes and platelets was studied in 24 normal men, using a double-blind, parallel study design. After a run-in period of 1 week, the subjects were treated with either placebo (n = 8) or 0.5 mg carmoxirole (n = 16) once daily for 1 week. Blood pressure and heart rate were not changed during carmoxirole administration in these normal men. Surprisingly, no significant effect of carmoxirole was found on the circulating plasma concentration of noradrenaline, adrenaline or dopamine. Other hormones such as renin, aldosterone and atrial natriuretic peptide were also not changed during carmoxirole administration. No significant effect of carmoxirole could be demonstrated on the intracellular concentration of Na+, K+, Mg2+ and Ca2+ and on the transmembrane fluxes of Na+ and K+ in erythrocytes and platelets. In the carmoxirole-treated subjects (n = 16), 6 subjects reported spontaneously adverse events such as syncope, dizziness and vomiting tendencies and/or fatigue.
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PMID:Erythrocyte and platelet cationic concentrations and transport systems in normal volunteers treated with carmoxirole. 790 90

We report on diagnostic and differential diagnostic considerations in the case of a 30 year old Italian woman with hypokalemic alkalosis, fatigue and muscular weakness. The symptoms were caused by a Bartter syndrome with distinctly increased renin but almost normal aldosterone levels in the serum and increased aldosterone values in the urine.
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PMID:[Hypokalemia in the course of a Bartter syndrome]. 801

Intact and adrenalectomized (ADX) rats were mildly food deprived and administered dexamethasone (type II agonist), aldosterone (type I agonist), corticosterone (mixed agonist), or vehicle 24 and 2 h prior to forced exercise in a treadmill. The endurance of intact animals was unaffected by hormone treatments. Adrenalectomy greatly advanced the onset of fatigue, and aldosterone exacerbated the effect of adrenalectomy. Corticosterone improved endurance in ADX rats, and dexamethasone was even more potent in this respect. Aldosterone slowed deprivation-induced weight loss in ADXs, while corticosterone and especially dexamethasone accelerated loss. Thus, endurance was directly related to body weight loss, and presumably to the fuels released by such loss. The results extend the type I-type II functional dichotomy to the delivery of utilizable energy for metabolically active tissues.
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PMID:Exercise endurance in rats: roles of type I and II corticosteroid receptors. 834 1

1. Heat acclimation was induced in eight subjects by asking them to exercise until exhaustion at 60% of maximum oxygen consumption rate (VO2) for 9-12 consecutive days at an ambient temperature of 40 degrees C, with 10% relative humidity (RH). Five control subjects exercised similarly in a cool environment, 20 degrees C, for 90 min for 9-12 days; of these, three were exposed to exercise at 40 degrees C on the first and last day. 2. Acclimation had occurred as seen by the increased average endurance from 48 min to 80 min, the lower rate of rise in the heart rate (HR) and core temperature and the increased sweating. 3. Cardiac output increased significantly from the first to the final heat exposure from 19.6 to 21.4 l min-1; this was possibly due to an increased plasma volume and stroke volume. 4. The mechanism for the increased plasma volume may be an isosmotic volume expansion caused by influx of protein to the vascular compartment, and a sodium retention induced by a significant increase in aldosterone. 5. The exhaustion coincided with, or was elicited when, core temperature reached 39.7 +/- 0.15 degrees C; with progressing acclimation processes it took progressively longer to reach this level. However, at this point we found no reduction in cardiac output, muscle (leg) blood flow, no changes in substrate utilization or availability, and no recognized accumulated 'fatigue' substances. 6. It is concluded that the high core temperature per se, and not circulatory failure, is the critical factor for the exhaustion during exercise in heat stress.
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PMID:Human circulatory and thermoregulatory adaptations with heat acclimation and exercise in a hot, dry environment. 848 4

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of torsemide are reviewed. Torsemide belongs to the pyridine-sulfonylurea class of loop diuretics. Its primary site of activity is the thick ascending limb of the loop of Henle, where it blocks active reabsorption of sodium and chloride, resulting in diuresis, natriuresis, and other effects. Torsemide has high bioavailability, a relatively long half-life, and a prolonged duration of activity. It is highly protein bound. Clinical trials indicate that torsemide is effective in the treatment of hypertension and of edema and other symptoms in patients with chronic renal failure (CRF), hepatic dysfunction, or congestive heart failure (CHF). Torsemide has infrequent, mild, and transient adverse effects; among the most common are orthostatic hypotension, fatigue, dizziness, and nervousness. The recommended initial oral dosages of torsemide are 10-20 mg/day for CHF, 20 mg/day for CRF, 5 mg/day for hypertension, and 5-10 mg/day (in combination with a potassium-sparing diuretic or aldosterone antagonist) for hepatic cirrhosis. In most patients, the pharmacokinetic advantages of torsemide over other loop diuretics are unlikely to translate into a substantial edge in clinical outcomes, and in practice there may be no cost advantages. Although torsemide does not offer major advantages over other loop diuretics, it may be of benefit in patients who do not respond to or cannot tolerate other agents.
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PMID:Torsemide: a new loop diuretic. 852 33

Hyperaldosteronism owing to aldosterone-producing adenoma (Conn syndrome) is a rare but potentially curable form of pediatric hypertension. The authors report on a 5-year-old girl who had symptoms of polyuria, polydipsia, and fatigue, and for whom the diagnosis of hyperaldosteronemia was suggested by a low serum potassium level and persistent hypertension. The diagnosis was confirmed by increased levels of plasma aldosterone and decreased levels of plasma renin. The tumor was localized with ultrasonography and computed tomography, which showed a 2-cm mass in the left adrenal gland. The left adrenal gland was excised, and pathological assessment showed an adenoma. Only 14 other pediatric cases (< 16 years of age) have been reported in the English-language literature.
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PMID:Conn syndrome in a child, caused by adrenal adenoma. 870 18


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