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

Systemic hemodynamic changes and noradrenaline concentrations in coronary sinus blood were studied at rest and during work before and after acute beta-receptor blockade. Patients with congestive cardiomyopathy were compared to patients with primary valvular diseases and to healthy subjects. Noradrenaline concentrations were higher in coronary sinus blood than in arterial blood and increased after beta blockade and during work. Noradrenaline concentrations were more increased in patients with more pronounced myocardial failure and did not seem to separate patients with congestive cardiomyopathy from those with valvular disease. Patients with congestive cardiomyopathy showed a good hemodynamic tolerance toward acute beta blockade.
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PMID:Effects of work and acute beta-receptor blockade on myocardial noradrenaline release in congestive cardiomyopathy. 4 91

A moderate elevation of the daily excretion of free noradrenaline and adrenalin is observed in chronic circulatory insufficiency, beginning with Stage IIA. The catecholamines metabolism is elevated, as shown by the daily excretion of normethanpherine and methanpherine and of vanillyl-mandelic acid. The activity of renin and angiotensinases was growing along with the progressing cardiac insufficiency. The blood level of angiotensinogen was decreasing, especially in patients with Stage IIB and III of decompensation. The daily excretion of aldosterone was growing along with the development of cardiac insufficiency. The functional state of the glucocorticoid function of the adrenal cortex was of a phased nature in cases of circulatory insufficiency. The study of the functional state of the epiphysis was conducted by way of determining the blood level of melatonine and of its daily excretion. In Stages I and IIA the level of this hormone was clearly elevated, in Stages IIB and III -- decreased as compared with the initial and normal levels. The plasma level of the antidiuretic hormone was distinctly growing, beginning with Stage IIB, reaching its maximal values in Stage III.
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PMID:[State of the neurohumoral regulatory system in circulatory insufficiency]. 18 17

Myocardial adenine nucleotides (nicotinamide adenine nucleotides included), glutathione, catecholamines (DOPA, dopamine, noradrenaline, adrenaline) and some enzymes in correlation were investigated in dogs with cardiac failure induced by bilateral iliac arteriovenous fistulas, and unilateral (left) heart vagotomy was also studied for its influence on the changes in the myocardial amounts of these compounds occuring in this pathological circumstance. The cardiac failure in arteriovenous fistula was characterized by the following myocardial metabolic aspects: (I) no change in the amount of proteins (although an important cardiac hypertrophy was present); (II) decreases in the amounts of adenine nucleotides (especially ADP and ATP), without significant variations in the adenosine concentration, accompanied by increases in the concentrations of nicotinamide adenine nucleotides (in both their oxidized and reduced forms) in the heart mitochondria; (III) no change in the amounts of oxidized and reduced glutathione and in the activity of NADH2-dependent glutathione reductase; (IV) a very significant increase in the activity of MAO without significant influences on the levels of the studied catecholamines. The partial vagal denervation of the heart was found to attenuate substantially the changes in the amounts of adenine nucleotides and nicotinamide adenine nucleotides in the myocardial mitochondria and to facilitate the action of MAO on noradrenaline leading to a significant decrease in its myocardial level.
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PMID:Role of the vagus nerves and catecholamines in the production mechanism of the myocardial failure induced by arteriovenous fistulas. 21 43

Patients with cardiac disorders have defective parasympathetic control of heart rate. To evaluate the possibility of similar changes in sympathetic control of heart rate, we compared reflex chronotropic responses to 80 degree upright tilt and nitroglycerin-induced hypotension in 31 cardiac patients and 7 normal individuals before and after partial parasympathetic blockade with atropine. Tilting revealed an attenuation of the normal heart rate increase in patients; the magnitude of this defect was greatest in patients with more severe symptoms (class III) and evidence of left ventricular dysfunction (the heart rate increase averaged 25 plus or minus 3 beats/min in normal subjects, 12 plus or minus 2 beats/min in class I-II patients, and 7 plus or minus 1 beats/min in class III patients). Class III symptoms due to mechanical causes (mitral stenosis), however, were not associated with this defect. A marked reduction in heart rate rise with hypotension was seen only in those class III patients without mitral stenosis (0.4 plus or minus 0.1 beats min-minus 1 mm Hg-minus 1 vs. 3.0 plus or minus 0.5 beats min-minus 1 mm Hg-minus 1 in normal subjects). This abnormality also persisted after atropine administration, thus confirming a defect in the sympathetic as well as the parasympathetic component of baroreceptor-mediated reflex heart rate control in patients with cardiac dysfunction. Infusions of isoproterenol produced equivalent rises in heart rate in patients and normal individuals, excluding a reduction in beta-receptor responsiveness as a cause of impaired sympathetic influence. Norepinephrine depletion, however, is a well-recognized concomitant of cardiac failure. It is possible that the reduction in sympathetically mediated heart rate responses results in part from depletion of the sympathetic neurotransmitter.
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PMID:Impairment of autonomically mediated heart rate control in patients with cardiac dysfunction. 80 57

In vitro experiments employing the polarographic technique of in-rush currents have demonstrated that adrenalin and noradrenaline in concentrations approaching those found in blood of myocardial infarction patients during the early days of the disease inhibit the tissue respiration of the cardiac muscle by 10--50%. A 10-minute intensive pain stimulation was found to inhibit the aerobic processes in the myocardium by 20--24%. Hypercatecholaminemia observed in the acute period of myocardial infarction is suggested to play an important role in the pathogenesis of cardiac insufficiency during myocardial infarction, since it causes histotoxic hypoxia of the intact portions of the cardiac muscle. The importance of eliminating the pain syndrome in patients with myocardial infarction and angina pectoris is emphasized.
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PMID:[Effect of exogenous catecholamines and pain action on the tissue respiration of the myocardium]. 85 43

Fifty patients with acute extensive myocardial infarction, with unfavourable course, were continuously survelled from the beginning of the disease till the terminal stage with the aim to study the interdependences between changes in the sympatho-adrenal and kallikrein-kinin systems in blood. The blood levels of adrenaline and noradrenaline were determined fluorometrically. The activity of the kallikrein-kinin system was estimated on the basis of three components: spontaneous esterase activity, prekallikrein activity, and kallikrein inhibitor activity in blood. Within the first six hours all patients had significantly elevated adrenaline and increased activity of the kallikrein-kinin system in blood. At 24h before death and during the terminal stage, in patients with acute heart failure and those with cardiogenic shock the adrenaline level gradually rose, and in patients with myocardial rupture the noradrenaline level increased. The activity of the kallikrein-kinin system remained elevated throughout the follow-up period. The application of findings as diagnostic and prognostic criteria in myocardial infarction is suggested.
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PMID:Changes in sympatho-adrenal and kallikrein-kinin systems in the terminal stage of extensive myocardial infarction. 92 53

In 20 normal persons and in 57 patients with heart diseases with functional class I-IV (according to the classification of the New York Heart Association) the 24 hour urinary excretion of the catecholamines adrenaline, noradrenaline and dopamine and of the O2-methylated degradation products metanephrine and normetanephrine was determined. The 3 catecholamines and the 2 O-methylated derivatives were measured simultaneously using chromatographic extraction and purification (Bio-Rex 70) and selective flurometric determination. The following results could be obtained: 1. The urinary excretion of noradrenaline increased with increasing severity of the heart disease. 2. In patients with severe congestive heart failure (functional class IV) in addition the adrenaline excretion in addition the adrenaline excretion increased significantly. 3. There was no relationship between the urinary excretion of dopamine and the severity of the heart disease. 4. The ratio of noradrenaline excretion to dopamine excretion increased with increasing severity of the heart disease, indicating an increased activity of dopamine-mu-hydroxylation in patients with congestive heart failure. 5. The excretion of the O-methylated degradation products metanephrine and normetanephrine in normal persons and in patients with heart diseases paralleled the excretion of the corresponding catecholamines adrenaline and noradrenaline. This indicates, that increased excretion of noradrenaline and adrenaline (Class IV) in patients with heart failure was not due to impaired catecholamine-degradation but indead to increased catecholamine-release indicating increased sympatho-adrenergic activity. These results show in addition that also in patients with heart failure O-methylation represents still the main degradation step for the inactivation of the circulating catecholamines. 6. The relationship of toal excretion of 0-methylated derivates to total excretion of adrenaline and noradrenaline, however, decreased with increasing severity of heart disease, indicating a relative impairment of O-methylation under the condition of severe congestive heart failure.
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PMID:[Urinary excretion of the catecholamines adrenaline, noradrenaline and dopamine as well as the derivatives metanephrine and normetanephrine in heart disease patients]. 101 4

15 patients have been treated with dopamine (2.0--6.0 gamma/kg/min) in the initial phase of cardiogenic shock after cardiac surgery. Indication was a systolic blood pressure of less than 85 mmHg associated with oligurie and peripheral vasoconstriction. 12 patients survived the cardiocirculatory crisis and the early postoperative period. Dopamine alone increased the arterial blood pressure in 6 patients from 52.4 to 80.1 mmHg and the urine flow from 25.2 ml/hr to 181.2 ml/hr. To obtain an optimal perfusion pressure additional application of Noradrenalin was used in 8 patients. In these patients the urine flow rose from 9.1 ml/hr to 131 ml/hr. In one patient no reaction, neither to dopamine, nor in combination with Noradrenalin was seen. The effect of pulse rate, central venous pressure and arterial oxygen tension has been discussed. Dopamine seems to be a useful substance in surgical patients with temporary cardiac insufficiency.
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PMID:[Clinical experiences with dopamine after heart surgery]. 108 Oct 33

Noradrenaline and adrenalin levels in different sections of the heart of persons deceased of myocardial infarction were measured, this being paralleled by determining the content of the said amines in the adrenal glands. It is shown that the noradrenaline level in the myocardium was down by comparison with controls during all periods of myocardial infarction studied. The most marked fall of the noradrenaline level in the heart muscle was noted to have occurred in persons who died in consequence of a progressive circulatory insufficiency. The authors believe that depletion of the noradrenaline reserves in the myocardium can be one of the causative factors in the development of cardiac insufficiency. An elevated concentration of adrenalin was found in the perinfarction region of the myocardium during acute period of infarction, especially 1-2 days following the onset of the latter. The highest rise in the adrenalin level was detected in individuals with repeated myocardial infarction evolving in a recurrent manner and complicated by well-marked arrhythmias. It cannot be ruled out that the amassment of adrenalin in the perinfraction zone may be causative of arrhythmias and recurrent lesions of the myocardium. In cases of myocardial infarction the catecholamines level in the adrenal glands is down, especially 1 more month following the development of infarction.
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PMID:[Noradrenaline and adrenaline content in different areas of the heart in patients dying of myocardial infarct]. 123 6

As soon as there is evidence of left ventricular dysfunction, even before clinical signs of chronic cardiac failure (CCF) have developed, intrinsic and extrinsic compensatory mechanisms are brought into play by the body. The majority of these mechanisms are under the influence of neurohumoral systems. When neurohormonal responses persist, as in CCF, they take on a beneficial nature since they participate in adaptation of the cardiovascular system as a whole, but they are also harmful since they worsen the working conditions of the myocardium by their cardiac and peripheral effects. Hyperactivity of the noradrenergic sympathetic nervous system is seen in CCF with levels 2 to 3 times higher as compared with subjects with normal left ventricular function. The circadian rhythm of catecholamines is modified. The increase in circulatory catecholamines is all the greater when cardiac failure is advanced. This release of noradrenaline (NA) is under the control of arterial baroreceptors which normally send to the central nervous system inhibitory inflow from the sympathetic nervous system. Inhibitory tone is released in case of a fall in blood pressure. Noradrenaline acts on beta-predominant myocardial receptors (inotropic and tachycardic) and alpha-predominant vascular receptors, resulting in arteriolar vasoconstriction. There is rapid onset of down regulation of myocardial beta-receptors. This fall essentially concerns beta 1, but beta 2 also, since they may be affected according to the etiology of CCF (ischemia). The Renin Angiotensin System (RAS) is also activated by the fall in systemic blood pressure. This consists of a cascade of reactions leading to the synthesis of angiotensin II responsible for powerful vasoconstriction of all arterial areas, including the coronary vessels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Metabolic changes in cardiac failure]. 130 Sep 20


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