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

Plasma concentrations of atrial natriuretic peptide and aldosterone and plasma renin activity were measured in patients with peripartum heart failure and in age matched healthy women post partum. Both groups had carried out traditional postpartum practices of salt consumption and body heating. Plasma concentrations (mean (SEM)) of atrial natriuretic peptide were significantly higher in the seven patients with peripartum heart failure (146.9 (24.3) pg/ml) than in the seven controls (4.4 (0.8) pg/ml). Both plasma aldosterone and plasma renin activity were suppressed in the patients with peripartum heart failure. After treatment for the heart failure plasma atrial natriuretic peptide fell considerably and there were associated increases in plasma aldosterone and plasma renin activity. The high plasma concentrations of atrial natriuretic peptide may have been a compensatory response to salt and water retention as well as to the heart failure. These high concentrations could also, in part, have suppressed the release of aldosterone and renin in an attempt to correct for volume overload.
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PMID:Atrial natriuretic peptide, aldosterone, and plasma renin activity in peripartum heart failure. 182 4

The pathophysiological role of atrial natriuretic factor in patients with chronic heart failure is still unclear. Plasma ANF levels are elevated in this condition, particularly in patients with severe left ventricular dysfunction and during acute exacerbations. Drug therapy, including diuretics, vasodilators and inotropes which reduce cardiac filling pressures also reduce plasma ANF levels. In the clinical setting the measurement of ANF levels may provide a useful means of assessing salt and water retention in patients with heart failure. Intravenous infusion of ANF to patients with heart failure causes a diuresis and natriuresis, a fall in filling pressures and possibly suppression of the renin-angiotensin aldosterone system. High bolus dosing with the peptide may reduce systemic vascular resistance resulting in hypotension, which markedly attenuates the renal effects. A new pharmacological approach in this area is the development of neutral endopeptidase inhibitors, which prolong the half-life of endogenous ANF and potentiate its effects. The therapeutic potential of ANF in heart failure has yet to be realised.
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PMID:Atrial natriuretic factor in chronic heart failure. 182 7

The potent diuretic and natriuretic properties of atrial natriuretic factor (ANF) suggest that atrial hormones may participate to the regulation of salt and water excretion under physiological conditions. ANF, via the increase of its intracellular second messenger cGMP, has been recently shown to inhibit the apical sodium channel of the inner medullary collecting tubule (IMCD). In addition, ANF inhibits renin and aldosterone synthesis and antagonizes the antinatriuretic effects of angiotensin II. ANF may also contribute to the excretion of free water by inhibiting both the secretion of vasopressin and its antidiuretic action. ANF appears to play an important physiological role in sodium repleted states, or when the effective plasma volume is increased. On the contrary, when the effective plasma volume is decreased or in sodium depleted states, the natriuretic effect of both endogenous and exogenous ANF is severely blunted. That ANF-resistance may be related to the activation of the renin-angiotensin-aldosterone axis, increased circulating catecholamines, renal sympathetic nerve stimulation, changes in renal hemodynamics or increased degradation of ANF. All these factors could explain the lack of significant natriuretic effect of both endogenous and exogenous ANF in some pathological conditions such as heart failure or liver cirrhosis. ANF may also been concerned in water homeostasis. In addition to the well-known osmoregulatory pathways of water metabolism, we recently found that ANF could be involved in the volume adjustment to acute water intake in normal man.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic factor and the endocrine control of electrolyte homeostasis. 183 42

The purpose of this investigation was to compare the chronic effects of converting enzyme inhibition with captopril to direct blockade of angiotensin II (AII) with DuP 753 in the rat model of heart failure. Rats with chronic heart failure postinfarction were treated for 2 weeks with either captopril (2 g/L, N = 9) in their drinking water or with DuP 753 (40 mg/kg/day for two weeks by gastric gavage, N = 10), or placebo (N = 9). At this dose, DuP 753 shifted the log dose-pressor response curve to AII parallel to the right by two orders of magnitude in both chronically treated normal and heart failure rats. In rats with heart failure, DuP 753 and captopril reduced left ventricular end-diastolic pressure from 26.7 +/- 1.5 to 14.2 +/- 3.0 (P less than .01) and 15.8 +/- 2.2 mm Hg (P less than .05), respectively, left ventricular end-diastolic volume index from 2.71 +/- 0.10 to 2.03 +/- 0.17 (P less than .05) and 2.18 +/- 0.15 (P less than .05), respectively; venous compliance increased from 2.27 +/- 0.06 to 2.80 +/- 0.18 (P less than .05) and 3.02 +/- 0.21 mL/mm Hg/kg (P less than .01), respectively. There were no significant changes in left ventricular weight/body weight ratio, mean aortic pressure, heart rate, or right atrial pressure. There was a trend, but not significant, for a reduction in total blood volume from 65.8 +/- 1.1 to 59.4 +/- 3.0 and 64.9 +/- 3.9 mL/kg, respectively. Thus, direct blockade of AII with DuP 753 or with converting enzyme inhibition with captopril produces similar hemodynamic changes in rats with heart failure after myocardial infarction.
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PMID:Hemodynamic effects of direct angiotensin II blockade compared to converting enzyme inhibition in rat model of heart failure. 185 61

In the treatment of heart failure ACE inhibitors gained a unique position because of their beneficial effect on prognosis. The most likely explanation is their influence on factors that determine progression of the disease. These are: progressive deterioration of central hemodynamics, impairment of coronary perfusion, further activation of vasopressor systems, imbalance of sodium and water homeostasis and occurrence of malignant arrhythmias. ACE inhibitors have been shown to modulate these factors in a positive manner. In addition, they may also act by modulating factors, which may exert harmful effects on cardiac function in long term. These are: prevention and regression of the hypertrophy of the left ventricle as well as the media of resistance vessels, prevention of restenosis following PTCA, prevention of cyclosporin-induced premature coronary artery sclerosis, and correction of an impaired glucose metabolism. Whereas the positive effects of ACE inhibitors in the treatment of heart failure are well documented, their value for preventing heart failure has not been established, yet.
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PMID:[ACE inhibition: mechanisms of cardioprotection in chronic heart failure]. 186 32

The RAS is part of an extremely powerful feedback system for long-term control of blood pressure and volume homeostasis. Disturbances that tend to lower blood pressure, such as heart failure, cirrhosis, and peripheral vasodilation, cause sodium and water retention until blood pressure returns to normal due, in large part, to the combined actions of ANGII and reduced arterial pressure. In response to increased sodium intake, decreased ANGII formation greatly amplifies the effectiveness of pressure natriuresis, thereby preventing large increases in body fluid volumes and blood pressure. In circumstances in which the RAS is inappropriately activated, the sodium retaining effects of ANGII necessitate increased blood pressure to maintain sodium balance via pressure natriuresis. Because the RAS is so powerful in regulating blood pressure, blockade of the system with ACE inhibitors offers a powerful therapeutic tool in diseases such as hypertension and congestive heart failure. The control of sodium excretion and blood pressure by ANGII is exerted through multiple intrarenal as well as extrarenal effects, including stimulation of aldosterone secretion, which can influence renal excretion. Current evidence suggests that the intrarenal effects of ANGII are quantitatively more important than those mediated by aldosterone in controlling blood pressure and renal excretion. The most important intrarenal effects of ANGII include efferent arteriolar constriction as well as direct effects on sodium transport. The constrictor effect on efferent arterioles also is important in preventing reductions in GFR in circumstances associated with impaired renal perfusion. Therefore blockade of ANGII formation in circumstances such as renal artery stenosis may caused marked reductions in GFR. However, in many patients efferent arteriolar vasodilation caused by ANGII blockade may not lower GFR markedly because of other autoregulatory mechanisms that compensate by causing parallel reductions in afferent arteriolar resistance. In these individuals, chronic ACE inhibition may prove to be beneficial in slowing the progression of renal disease because a reduction in glomerular hydrostatic pressure may help to prevent glomerular damage.
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PMID:The renin-angiotensin system: renal actions and blood pressure regulation. 187 29

Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome, and pregnancy. Nonosmotic vasopressin release has been implicated in the water retention of these edematous disorders. The nonosmotic release of vasopressin is consistently associated with activation of the sympathetic nervous and renin-angiotensin-aldosterone systems in both experimental animals and in edematous patients. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin and activation of the renin-angiotensin system. These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. Neither total extracellular fluid volume nor blood volume is a determinant of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by a decrease in effective arterial blood volume (EABV) due to either a fall in cardiac output or peripheral arterial vasodilation. The acute response to a decrease in EABV 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 resultant renal vasoconstriction 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:Unifying hypothesis of sodium and water regulation in health and disease. 193 81

Increased sympatho-adrenergic activity is a compensatory mechanism in cardiac failure. Accordingly, beta-receptor blockers are generally regarded as contraindicated for use in heart failure. In 1975, Waagstein reported the first successful use of beta-receptor blockers in patients with idiopathic dilated cardiomyopathy. It was shown that the prognosis of patients with dilated cardiomyopathy could be improved by beta-receptor blockade. In this regard, most experience is associated with metoprolol. It should be stressed that the initial, and long-term dosage, as well, was maintained at a very low level (beginning, for example, with 6.25 mg metoprolol daily). An on-going, international, multicenter study is intended to clarify which patients with dilated cardiomyopathy may benefit from treatment with beta-receptor blockers. Additionally, further information is anticipated with respect to the complex mechanism of action. Beside the direct cardiac action with blockade of the cardiotoxic effect of the extremely high levels of plasma catecholamines, induction of an upregulation of the down-regulated beta-1-receptors there is attenuation of the activity of the renin-angiotensin-aldosterone system. Overall, this leads to interruption of the vicious cycle of maladaption associated with chronic heart failure and its attendant unfavorable vasoconstriction and sodium and water retention. This positive aspect of beta-1-receptor blockade in dilated cardiomyopathy carries with its initially and unavoidable negative inotropic effect and thus, in the individual patient, the net effect is difficult to predict. Consequently, the indication must be established on an individual basis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Sympathetic activity in patients with heart failure due to idiopathic dilated cardiomyopathy: modification by beta receptor blockers--a therapeutic approach?]. 197 15

Extracorporeal circulation can be utilized successfully to rewarm accidental hypothermia victims. This paper describes a 51 year-old man who had been immersed in cold sea water for about 45 minutes. At the time of rescue his ECG was isoelectric. The core temperature was 27 degrees C. Cardiopulmonary resuscitation was performed for 190 minutes before extracorporeal circulation was established. Without active surface rewarming the temperature had dropped to 24 degrees C. Biventricular heart failure became evident during rewarming. Sternotomy and pericardiotomy were carried out to exclude cardiac tamponade, which was not found. After two hours of reperfusion the patient could be weaned from bypass supported by high-dose vasopressor infusion. He was extubated the following day. He was discharged after 12 days without any signs of permanent damage to organs.
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PMID:[Deep accidental hypothermia with asystole. A successful treatment with heart-lung machine after prolonged cardiopulmonary resuscitation]. 199 75

We reported a 29-year-old man with active endocarditis complicating aortic and mitral valve regurgitation. The echocardiogram showed a mycotic aneurysm at aortic valvular annulus and a aneurysm of mitral valve. Heart failure was progressive and caused anuria. Prior to emergent double valve replacement, 2,500 ml of water was removed. Then hemodynamics became stationary. Urination was good during and after operation. In this case, complicating acute renal failure, dehydration with extracorporeal ultrafiltration method was very effective for improvement of hemodynamics.
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PMID:[An emergent aortic and mitral valve replacement for active infective endocarditis preoperatively using extracorporeal ultrafiltration method]. 202 Jan 51


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