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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical and laboratory features of 18 adult pellagrins are reviewed. Only four patients (22%) had the full trial of dermatitis, diarrhea and dementia. Dermatitis alone occurred in six(33%), dementia in five(28%) and dermatitis and diarrhea in three(17%). In one patient, dermentia was the initial sign of a relapse. Steatorrhea was found in six patients and was usually associated with marked alopecia. Edema without evidence of cardiac failure was present in seven patients. A diffuse increase in slow wave activity on the electroencephalogram was characteristic in patients with dementia. Fever occurred in 14 patients, and an infection was documented in 10 of these. Common laboratory abnormalities included a normochromic, normocytic anemia, lymphopenia, eosinopenia hyperuricemia, and low serum levels of albumin, urea, cholesterol, carotene, potassium, calcium, and magnesium. Adrenal and thyroid function were normal, but a low serum T4, high serum free T4, and an elevated T3 resin uptake were frequently observed. These abnormalities were corrected with treatment of the underlying nutritional disorder. In two patients initially treated with thiamine alone, and in one who received inadequate amounts of niacin and protein, there was marked deterioration of mental function, which responded to administration of niacin and proper diet.
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PMID:Pellagra: an analysis of 18 patients and a review of the literature. 86 2

As a prelude to a study of severe ischemic heart failure, the therapeutic response of the ischemic ventricle to epinephrine and acetylstrophanthidin in nontoxic doses was determined in 24 intact anesthetized dogs undergoing a first episode of acute regional ischemia. A thrombotic obstruction was produced in the left ventricular dysfunction. The elevation of end-diastolic pressure and reduced stroke volume in control dogs were not significantly altered by administration of strophanthidin. Epinephrine (0.05 mug/kg per min) elicited a significant reduction in end-diastolic pressure and increase in stroke volume. The latter was not attended by an increased incidence of ventricular fibrillation, whereas fibrillation occurred in half of the group given strophantihidin. Thus, the catecholamine was selected to study pump failure. Severe ischemic heart failure was assessed in two groups with scar from previous infarction for up to 4 hours. By 60 minutes of ischemia the increase in end-diastolic pressure and volume and decrease in stroke volume and ejection fraction were comparable in both groups. Thereafter, alternate animals received small doses of epinephrine (0.05 to 0.15 mug/kg per min) with graded increments at 60 minute intervals to counter tachyphylaxis and findings were compared with those in control dogs. Over the subsequent 3 hours, there was progressive deterioration of left anterior descending coronary artery, affecting ventricular function in the untreated group with an increase in end-diastolic pressure from 10 plus or minus 1 to 33 plus or minus 2.4 mm Hg. End-diastolic volume increased by 63 percent; stroke volume and ejection fraction decreased by 48 and 66 percent, respectively. The infusion of epinephrine was attended by a significantly lower end-diastolic pressure of 20 plus or minus 2.5 mm Hg, whereas end-diastolic volume, stroke volume and ejection fraction were restored to control levels after 4 hours of ischemia. Mortality in the untreated group was 62 percent by 4 hours; all seven animals in the treated group survived.
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PMID:Ischemic heart failure: sustained inotropic response to small doses of I-epinephrine without toxicity. 111 1

Adrenaline, noradrenaline and dopamine excretion was investigated in essential hypertension (n = 20), atherosclerotic heart failure (n = 20, NYHA class II and III), chronic angina (n = 10) and in healthy controls, in four time intervals: between 600-1200, 1200-1800, 1800-2400, 2400-600. Fluorimetric method of Anton and Sayre was employed. In patients with essential hypertension the circadian rhythm of adrenaline, noradrenaline and dopamine excretion was maintained but in all time intervals excretion of dopamine was decreased. In individuals with congestive heart failure due to atherosclerosis and in patients with ischemic heart disease, physiological circadian rhythm of adrenaline and noradrenaline excretion was found to be abolished. This was not the case with dopamine excretion which was undisturbed.
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PMID:[Hypertension, heart failure and angina pectoris. Diurnal rhythm of urinary excretion of catecholamines]. 164 Jun 65

Radiotracer methods were used to measure the rates of regional release of adrenaline and noradrenaline into plasma in man. This was done as a partial test of a theory of essential hypertension pathogenesis which envisages an important cotransmitter function for neuronally released adrenaline. In healthy resting men no release of adrenaline could be detected from the heart, lungs or liver. Adrenaline was released into the right renal vein but an adrenal medullary source is suspected. With the relatively limited activation of the cardiac sympathetic outflow which accompanied mental challenge and isometric exercise, cardiac adrenaline release remained undetectable. During supine bicycle exercise, which increased cardiac noradrenaline release 10-30 fold, to a mean value of 197 ng/min, cardiac adrenaline release averaged 2.36 ng/min. In two clinical conditions associated with persistently elevated plasma adrenaline concentrations, cardiac failure and adrenaline-secreting phaeochromocytoma, regional release of adrenaline was clearly evident. Thus, in normal man during exercise, and in patients with cardiac failure at rest, adrenaline is released from non-adrenal sources, and probably from sympathetic nerves. Whether neuronal adrenaline release of the degree found would be sufficient to facilitate noradrenaline release, augment sympathetically-mediated cardiovascular responses and contribute to the development of arterial hypertension remains to be tested.
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PMID:Is adrenaline released by sympathetic nerves in man? 182 56

The stimulant effects of adrenaline and noradrenaline on contractile force and adenylate cyclase, mediated through beta 1 and beta 2-adrenoceptors, are analysed in isolated atrial and ventricular myocardium of man. The tissues were obtained from patients without advanced heart failure undergoing heart surgery. Usually, both adrenaline and noradrenaline stimulated adenylate cyclase predominantly through ventricular and atrial beta 2-adrenoceptors. Because the relative density of beta 2-adrenoceptors is usually smaller than that of beta 1-adrenoceptors, stimulation of one beta 2-adrenoceptor leads to the production of up to 10 times more cyclic AMP molecules than does stimulation of one beta 1-adrenoceptor. Adrenaline and noradrenaline maximally enhance contractile force through both atrial and ventricular beta 1-adrenoceptors. Adrenaline can also maximally enhance contractile force through atrial beta 2-adrenoceptors. In the ventricle, adrenaline increases force via beta 2-adrenoceptors by up to 60% of its maximal beta 1 response. Noradrenaline can increase atrial and ventricular contractile force through beta 2-adrenoceptors but only at high concentrations. Unexpectedly, in atria from patients treated with the beta 1-selective antagonist atenolol, contractile responses to adrenaline are markedly and selectively augmented through activation of beta 2-adrenoceptors. In atria from atenolol-treated patients equi-inotropic concentrations of adrenaline and noradrenaline acting through beta 2 and beta 1-adrenoceptors, respectively, cause similar increases of cyclic AMP and of cyclic AMP-dependent protein kinase activity.
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PMID:A comparison of the effects of adrenaline and noradrenaline on human heart: the role of beta 1- and beta 2-adrenoceptors in the stimulation of adenylate cyclase and contractile force. 257 19

In this study plasma levels of atrial natriuretic peptide and of the catecholamines epinephrine and norepinephrine were investigated in hypertensive patients (HT) (n = 30). 22 normotensive patients (NT) served as controls. Hypertensives showed an elevated ANP-level in comparison with controls (46.8 +/- 3.3 vs. 36.8 +/- 3.3 pg/ml, M +/- SEM, p less than 0.01). When patients with myocardial infarction or with reduced ejection fraction were excluded, the same relation was demonstrated (49.3 +/- 3.2 vs. 33.6 +/- 2.0 pg/ml, p less than 0.01). Plasma norepinephrine was 230.8 +/- 52.3 pg/ml in HT compared with 138.0 +/- 19.6 pg/ml in NT (p less than 0.05). Epinephrine was 70.8 +/- 10.5 vs. 54.8 +/- 9.7 pg/ml in HT and NT. To exclude an increased left ventricular enddiastolic - and hence left atrial - pressure as the cause for the elevation of ANP and norepinephrine, HT and NT were matched for the same levels of enddiastolic pressure (LVEDP) (n = 18). For each level of LVEDP ANP was higher in HT than in NT (p less than 0.01). The same held true for norepinephrine (p less than 0.05) and to a lesser extent for epinephrine (p = 0.09). Our results demonstrate that patients with essential hypertension exhibit markedly elevated levels for ANP and catecholamines which is not due to myocardial failure. We propose that the increased secretion of the vasodilatory hormone ANP serves as counterregulation against the vasoconstrictor norepinephrine. The endocrine function of the heart may play a pivotal role in the modulation of sympathetic activity.
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PMID:[Elevated levels of atrial natriuretic peptide and plasma catecholamines in arterial hypertension--indications for an interaction]. 297 96

Changes in contraction amplitudes, contraction peak time and relaxation time were evaluated at 50% and 80% of contraction peak, with adrenaline or strophanthin acting on the myocardium pretreated with antiarrhythmic substances, using atrial specimens from patients with acquired heart diseases and septal defects. Etmozin and ethacizine were shown to have a negative inotropic effect, reducing contraction intensity by about 50%. Adrenaline and strophanthin are capable of restoring myocardial contractility in the presence of antiarrhythmic effects without actually inducing spontaneous auto-arrhythmic activity. Causes of the recovery of myocardial mechanical activity, effectuated by adrenaline or strophanthin in the presence of antiarrhythmic agents are discussed. It is suggested that a combination of effective antiarrhythmic properties and negative inotropic effect of phenothiazines is significant for cases of arrhythmias with and without signs of heart failure.
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PMID:[Effect of the anti-arrhythmia compounds etmozin and ethacizine on the contractile activity of myocardial preparations from heart defect patients]. 330 27

Interaction between kininase II and anaesthesia is not well described. Twenty two patients treated by kininase II for congestive heart failure are studied during anaesthesia for cardiovascular surgery. A first group of seventeen homogeneous hemodynamic data are reported. High cardiac index contrasts with severe clinical cardiac failure. A second group of inhomogeneous patients are separately described. Vasoconstrictor can be codified in the situation of low systemic resistance with high cardiac index. Preoperative treatment can be continued, under requirement of hemodynamic monitoring.
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PMID:[Is it necessary to discontinue captopril before heart surgery?]. 355 42

The effects of enalapril on exercise capacity and neurohumoral factors during exercise were evaluated in 10 patients with heart failure. Echocardiograms and exercise testing with expired gas analysis were performed before and after enalapril. Blood samples were obtained before and after exercise. Both ejection fraction and percent fractional shortening increased with enalapril (p < 0.05). The anaerobic threshold and peak VO2 did not change with enalapril. Epinephrine and norepinephrine levels at peak exercise decreased with enalapril (p < 0.1). Plasma renin both at rest and at peak exercise increased with enalapril (p < 0.1). Angiotensin II was lower after enalapril both at rest and at peak exercise (p < 0.1 and p < 0.05, respectively). Aldosterone was lower after enalapril both at rest and at peak exercise (p < 0.05). Atrial natriuretic peptide (ANP) was lower after enalapril both at rest and at peak exercise. There was no significant correlations between peak VO2 and changes in neurohumoral factors before and after enalapril during exercise. In conclusion, neurohumoral changes with enalapril occurred during exercise even if exercise capacity did not improve. Moreover, the improvement of cardiac function at rest and neurohumoral factors with enalapril did not lead to a change of exercise capacity.
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PMID:Effects of enalapril on the exercise capacity and neurohumoral factors during exercise in patients with chronic heart failure. 896 Jun 18

Adrenaline and noradrenaline exert their effects via specific adrenergic receptors. Of the nine known subtypes of these receptors, the beta 1-subtype mediates an increase in cardiac contractility, while the beta 2-subtype is responsible for vasodilatation. These receptors are not just simple signal transducers but components of a complex and highly regulated signalling machinery. A loss of sensitivity of this machinery may be induced by exogenous as well as endogenous stimuli (= desensitisation). Desensitisation of cardiac beta-adrenergic receptors may contribute to contractile dysfunction in chronic heart failure.
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PMID:[Mechanisms of the regulation of adrenergic beta-receptors]. 908 78


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