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

We studied the hemodynamic effects of vasopressin and the renin-angiotensin system in an animal model of high output heart failure in conscious rats (aorto-caval fistula). We found significantly elevated levels of plasma renin concentration (p less than 0.025), norepinephrine (p less than 0.02), and up to 4 to 5 times higher values of vasopressin (p less than 0.002) in the rats with heart failure as compared with control animals. In contrast to the control rats that had a normally functioning osmoreceptor system, we found an inverse relationship between plasma osmolality and arginine vasopressin in the rats with heart failure in association with edema. Using a specific antagonist of the pressor activity of vasopressin, we found no significant effect on heart rate, mean arterial pressure, cardiac output (thermodilution), and peripheral vascular resistance in the control animals and in the rats with aorto-caval fistula. Captopril resulted in a significant fall of mean arterial pressure in the rats with shunt (p less than 0.001). The coincidence of high values of vasopressin and, in a number of animals, low plasma osmolalities and edema suggests a role of vasopressin in the formation of edema and in the development of "dilutional hypo-osmolality."
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PMID:Vasopressin and renin in high output heart failure of rats: hemodynamic effects of elevated plasma hormone levels. 258 Jan 26

Isolated ultrafiltration was performed in 107 patients with refractory heart failure (HF) which developed in the presence of different cardiovascular diseases. The beneficial action of isolated ultrafiltration in 71 patients (68%) with refractory HF was determined by complex interaction of the effects provoked by ultrafiltrate removal. Among those effects of paramount importance was correction of secondary hyperaldosteronism and reduction of the concentration of antidiuretic hormone accompanied by the improvement of liver and heart functions.
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PMID:[Isolated ultrafiltration of the blood in patients with refractory heart failure: the status of the renin-angiotensin-aldosterone system and the secretion of antidiuretic hormone]. 258 72

The renin-angiotensin-aldosterone system plays an important role in the development of congestive heart failure (CHF). In patients with chronic heart failure, angiotensin-converting enzyme (ACE) inhibitors, such as captopril, enalapril, and quinapril, have been shown to improve hemodynamics, reduce symptoms of fatigue and dyspnea, increase exercise capacity, correct hyponatremia, reduce diuretic requirements and ventricular arrhythmias, and conserve potassium and magnesium. ACE inhibitors reduce circulating levels of angiotensin II and aldosterone and may reduce plasma norepinephrine and vasopressin levels. They are equally effective in patients with mild to moderate heart failure and in patients with severe cardiac impairment. ACE inhibitors are at least as beneficial as digitalis in patients with mild heart failure, and they may even be considered as first-line therapy. Promising results have also been obtained in patients with myocardial infarction, in whom long-term therapy with ACE inhibitors has prevented an increase in heart size. ACE inhibitors improve prognosis in patients with severe heart failure and in patients with hyponatremia; the question of effect on survival in mild to moderate heart failure has yet to be answered.
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PMID:ACE inhibitors in congestive heart failure. 267 Feb 20

A number of theoretical and practical aspects of acute myocardial infarction suggest a potential role for ACE inhibition in enhancing coronary blood flow and limitation of infarct size. Indeed, the use of ACE inhibitors in acute myocardial infarction could be viewed as a logical intervention in the face of the neuroendocrine response which accompanies the acute phase. During the first 24 h post-infarction, very high plasma concentrations of arginine-vasopressin and catecholamines occur. This is followed by a sharp rise in the concentration of angiotensin II (ANG II) over the next few days. The neuroendocrine response is most marked in those patients with larger infarcts, who frequently develop left ventricular failure. The extent to which these factors influence coronary flow in acute myocardial infarction is unknown, although in chronic heart failure ACE inhibition does not reduce coronary blood flow despite a reduction in rate-pressure product, suggesting a coronary vasodilator effect. However, in the presence of fixed coronary stenoses, the fall in blood pressure and, therefore, of coronary perfusion pressure must be taken into account. Whether or not the use of ACE inhibitors can limit infarct size in man also remains to be determined, although it has been clearly demonstrated that concentrations of ANG II similar to those observed in the early phase of myocardial infarction can cause myocardial cell damage in experimental animals. Post-infarction ventricular enlargement can be reduced by ACE inhibitors. Additionally, ACE inhibitors, through their balanced vasodilator effect, maintain cardiac output whilst reducing filling pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of angiotensin-converting enzyme inhibition on coronary blood flow and infarct size limitation. 267 35

The positive action exerted by isolated ultrafiltration on 69 patients with refractory heart failure was shown to be due to the complex interaction of effects produced by ultrafiltrate removal. Among the effects, a leading role is played by therapy for hyperaldosteronism and reduction of antidiuretic hormone levels along with improvement of the functional status of the liver and heart.
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PMID:[Effect of isolated ultrafiltration on plasma hormone levels in patients with heart failure resistant to drug therapy]. 268 56

Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome and pregnancy. In recent years the use of a sensitive radioimmunoassay for plasma vasopressin has implicated the role of nonosmotic vasopressin release in the water retention of these edematous disorders. In experimental studies and studies in humans it has been found that the nonosmotic release of vasopressin is consistently associated with activation of the sympathetic nervous and renin-angiotensin-aldosterone systems. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin (carotid and aortic baroreceptors) and activation of the renin-angiotensin system (renal beta-adrenergic receptors). These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. In this context neither total extracellular fluid (ECF) volume nor blood volume are determinants of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by either a fall in cardiac output (e.g. ECF volume depletion, low-output cardiac failure, pericardial tamponade or hypovolemic nephrotic syndrome) or peripheral arterial vasodilation (e.g. high-output cardiac failure, cirrhosis, pregnancy, sepsis, arteriovenous fistulae and pharmacologic vasodilators). With a decrease in effective arterial blood volume (EABV), initiated by either a fall in cardiac output or peripheral arterial vasodilation, the acute response involves vasoconstriction mediated by angiotensin, sympathetic mediators and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The renal vasoconstriction which accompanies those states that decrease EABV, by either decreasing cardiac output or causing peripheral arterial vasodilation, limits the distal tubular delivery of sodium and water thus maximizing the water-retaining effect of vasopressin and impairing the normal escape from the sodium-retaining effects of aldosterone. The elevated glomerular filtration rate and filtered sodium load in pregnancy allows increased distal sodium and water delivery in spite of a decrease in EABV, thus limiting edema formation during gestation.
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PMID:Pathophysiology of vasopressin in edematous disorders. 269 4

An inappropriate antidiuretic hormone secretion (SIADH) has been recognized as the cause of hypotonic hyponatremia, and the occurrence of this syndrome, accompanied by an ADH-producing adenocarcinoma in the nasal cavity, is reported. In February, 1987, a 50-year-old male, showing sights of delirium, disorientation, and irritability was admitted to the hospital. The patient was observed to be healthy, except for a neck lymphnode metastasis that was present up to the time of his hospitalization. The hyponatremia was incidentally found, although dehydration or intravascular volume depletion were not noted. These neuropsychiatric symptoms were considered to be associated with hyponatremia due to SIADH. He had had a partial maxillectomy, a neck dissection, and irradiation to the nose and nasal cavity 32 months earlier, and then underwent a surgical resection of the neck metastasis; he had a total of 10 other operations before the onset of the symptoms. Upon initial inspection, since neither an intracranial invasion nor a brain metastasis was found, we diagnosed that his symptoms were due to an autonomic disturbance caused by surgical and mental "stress". When he died of cardiac failure due to a mediastinal invasion 8 months after the onset of SIADH, tumor tissues was extirpated in an autopsy and was then cultured. In this manner, it was proved that the tumor cells had been producing ADH. This procedure clarified that the syndrome had resulted from an ADH-producing tumor of the nasal cavity.
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PMID:[A case of adenocarcinoma of the nasal cavity associated with syndrome of inappropriate secretion of antidiuretic hormone(SIADH)]. 277 60

The biochemical abnormalities associated with heart failure include dysfunction of contractile proteins, functional impairment of energy-linked enzymes and disruption of cell membrane structure. The haemodynamic impairment resulting from cardiac dysfunction activates several neurohormonal systems, notably the renin-angiotensin-aldosterone system, sympatho-adrenal system and vasopressin release, whilst clinically important factors include an enlarged heart, increased systolic wall stress and an increased myocardial oxygen demand. An inverse relationship exists between systolic wall stress (afterload) and contractile function in heart failure. Moreover the increased systolic wall stress that occurs as a result of reduced cardiac output raises myocardial oxygen consumption, causing cardiac function to deteriorate still further. Diastolic abnormalities play an important role in hypertrophic disorders, in ventricular dilatation and in cases of myocardial ischaemia. The therapeutic objectives are therefore to decrease heart size, to reduce wall stress and oxygen demand, and to enhance diastolic distensibility.
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PMID:Contractile, haemodynamic and neurohormonal abnormalities in heart failure. 280 88

By means of specific inhibitors of the renin-angiotensin system (captopril) and of the sympathetic nervous activity (prazosin) in dogs with congestive heart failure, and by using a specific antagonist of the pressor activity of arginine vasopressin in rats with heart failure, we studied the influence of these pressor hormone systems on peripheral vascular resistance and cardiac function. All three humoral vasoconstrictor systems were stimulated in heart failure. The experiments in dogs showed that the renin-angiotensin system plays an important role in the pathogenesis of heart failure by increasing peripheral vascular tone, thus impairing cardiac function, a mechanism which could be nearly completely prevented by converting enzyme inhibition. The increased sympathetic nervous activity was only insignificantly attenuated by the converting enzyme inhibition and its contribution to the increase of peripheral vascular resistance was only small and transient. The rats with heart failure showed no effect on the vasopressin inhibitor on peripheral vascular resistance and cardiac function, despite plasma vasopressin levels which were 4 to 5 times higher than those in control animals. The inappropriately high secretion of vasopressin in relation to a decreased plasma osmolality may have contributed to the formation of edema and to the development of 'dilutional hypoosmolality'.
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PMID:Neurohumoral vasoconstrictor systems in heart failure. 286 48

Alterations in the peripheral circulation by influencing aortic impedance and venous capacitance have a remarkable effect on cardiac performance in patients with left ventricular dysfunction. Systemic vasoconstriction in heart failure is influenced by activation of the sympathetic nervous system (increased plasma norepinephrine), the renin-angiotensin system (increased PRA) and the antidiuretic hormone system (increased arginine vasopressin). The level of plasma norepinephrine is related weakly to the severity of resting left ventricular dysfunction and strongly to the subsequent risk of mortality. Attenuation of reflex responsiveness to low pressure mechanoreceptors (orthostatic tilt) and to carotid and aortic baroreceptors (nitroprusside infusion) occurs in heart failure and the degree of abnormality also may be related to mortality. Vasodilation with consequent improvement in left ventricular function may be accomplished by non-specific dilators (nitroprusside, nitrates, hydralazine, nitrendipine) or by specific interference with neurohumoral mechanisms (sympathetic blockade, converting enzyme blockade, AVP blockade). Plasma norepinephrine may be reduced by central or presynaptic mechanisms (guanabenz, bromocriptine, captopril). The hemodynamic effect of this anti-sympathetic effect appears to be related to the relative influence on cardiac vs. peripheral sympathetic tone and/or concomitant effects of the drugs. Long-term trials are needed to determine whether chronic inhibition of the sympathetic nervous system will have a salutary effect on the hemodynamics, symptomatology and prognosis of cardiac failure.
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PMID:Nervous system control mechanisms in heart failure. 287 90


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