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

Arginine vasopressin levels in 17 neonates with cardiac disease were compared with control levels in 10 healthy newborn infants. Infants with congestive heart failure who were free of left ventricular outflow tract obstruction had a mean level of 80 +/- 18 pg/ml, which was significantly greater than the mean control level (p less than 0.001). Infants with congestive heart failure and left ventricular outflow tract obstruction had a mean vasopressin level of 3 +/- 0.7 pg/ml, which was lower than the mean control level of 6 +/- 0.7 pg/ml (p less than 0.05). The data suggest that impaired forward flow to high pressure sinoaortic and ventricular baroreceptors is necessary for vasopressin release in congestive heart failure. In left ventricular outflow tract obstruction with heart failure these receptors may be impaired or absent, leading to decreased vasopressin release. Low plasma arginine vasopressin may adversely affect circulatory homeostasis.
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PMID:Variable arginine vasopressin levels in neonatal congestive heart failure. 334 66

The extent of neuroendocrine activation, its time course, and relation to left ventricular dysfunction and arrhythmias were investigated in 78 consecutive patients with suspected acute myocardial infarction. High concentrations of arginine vasopressin were found within six hours of symptoms, even in the absence of myocardial infarction (n = 18). Plasma catecholamine concentrations also were highest on admission, whereas renin and angiotensin II concentrations rose progressively over the first three days, not only in those with heart failure but also in patients with no clinical complications. Heart failure, ventricular tachycardia, and deaths were associated with extensive myocardial infarction, low left ventricular ejection fraction, and persistently high concentrations of catecholamines, renin, and angiotensin II up to 10 days after admission, whereas in uncomplicated cases concentrations had already returned to normal.
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PMID:Neuroendocrine activation after acute myocardial infarction. 341 70

Cardiac (or myocardial) failure, a major health problem, can be defined using physiologic criteria that consider the adequacy of O2 delivery relative to the body's O2 requirements. In clinical terms, cardiac failure may be described in terms of its chronicity or the extent to which signs and symptoms of right- versus left-sided heart failure are dominant. Congestive heart failure is a clinical syndrome that consists of a constellation of signs and symptoms that arise from congested organs and hypoperfused tissues. Acute cardiac failure occurs because of a decrease in myocardial contractility that can be offset by the Frank-Starling mechanism. In chronic cardiac failure dilatation and myocardial hypertrophy serve to restore ventricular function. Other compensatory responses that are invoked include a salt avid kidney, which mediates an expansion of the intravascular space, and the activation of the adrenergic nervous and renin-angiotensin-aldosterone systems and an increase in circulating arginine vasopressin. The management of acute and chronic cardiac failure can be derived from an understanding of the pathophysiologic mechanisms responsible for their appearance and include improving cardiac performance, as well as the distribution of systemic blood flow to tissues based on physiologic priorities and moment to moment variations in O2 requirements.
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PMID:Pathophysiology of acute and chronic cardiac failure. 361 18

The aims of this study were to investigate the influence of heart failure and dietary sodium content on the natriuretic effect of furosemide. Ten healthy Golden Syrian hamsters (HH) and 10 hamsters with a cardiomyopathy (CMH) were maintained on a normal sodium diet (NSD) and an equal number of animals on sodium deficient diet (SDD) for a minimum of 40 days. Three experiments were conducted on days 1, 20 and 40. Each experiment started with a 24-hour urine collection (control), followed by the administration of 5 mg/kg of furosemide i.p. and a second 24-hour urine collection and finally, the administration of 2 mg/kg of indomethacin i.p. followed 30 minutes later by 5 mg/kg of furosemide and a 24-hour urine collection as well as blood sampling. Sodium, creatinine, furosemide and arginine vasopressin (AVP) were measured in the urine and sodium, creatinine and AVP in plasma. After 134 days on a SDD, four HH resumed a NSD and the response to furosemide was again assessed after 12 days. Our results indicate that the natriuretic response to furosemide is higher in CMH than in HH. The SDD tended to increase the response to furosemide in HH as well as in CMH. Indomethacin did not influence the response to furosemide under any experimental condition. In four HH the increment in the fractional excretion of sodium in response to furosemide was 0.88 +/- 0.21% after 134 days on SDD and decreased to 0.35 +/- 0.12 (p less than 0.05) after 12 days on NSD. In all cases urinary excretion of furosemide was similar. Plasma AVP was higher in CMH and was not influenced by the SDD. In conclusion, SDD as well as cardiomyopathy with congestive heart failure do not decrease the natriuretic effect of furosemide and may not be a cause in the variability of the natriuretic response to furosemide.
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PMID:Influence of heart failure and sodium content in the diet on the natriuretic response to furosemide in hamsters. 390 71

The incidence of congestive heart failure is increasing in the United States. This common syndrome is characterized not only by impaired ventricular function but also by an increase in some endogenous vasoconstrictor substances, including norepinephrine, angiotensin II, and arginine vasopressin. Although activation of the systems that release these substances is presumed to be compensatory (to maintain perfusion pressure during inadequate flow), the sympathetic nervous system, renin-angiotensin-aldosterone system, and arginine vasopressin may contribute to the pathogenesis of the syndrome. The excessive vasoconstriction present in heart failure likely produces a further burden on the failing myocardium. New strategies in therapy are being developed to counteract the activation of vasoconstrictor forces in congestive heart failure. Data indicate that selective blockade of the renin-angiotensin system is useful. Preliminary data suggest that inhibition of the sympathetic nervous system may be helpful, and inhibition of vasopressin in animals with heart failure is being studied. New and more selective therapy for heart failure may come from these studies.
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PMID:The neurohumoral axis in congestive heart failure. 614 9

Arginine vasopressin, a potent vasoconstrictor and regulator of body water, is frequently increased in the plasma of patients with congestive heart failure. Other neurohumoral control networks, such as the sympathetic nervous system and the renin-angiotensin system, also demonstrate increased activity in congestive heart failure, but fail to respond normally to physiologic stress, such as orthostatic tilt. To assess the response of plasma vasopressin to orthostasis in heart failure, vasopressin was measured before and at 10 and 45 minutes during passive upright tilt in 15 patients with congestive heart failure and their response was compared with that in 9 normal control subjects. Arginine vasopressin was measured by radioimmunoassay. In the normal subjects, plasma arginine vasopressin was 5.3 +/- 2.3 pg/ml at control, was unchanged at 10 minutes, but significantly increased to 7.0 +/- 2.5 pg/ml at 45 minutes (p less than 0.05). In contrast, patients with congestive heart failure showed no significant changes in arginine vasopressin levels from the control levels of 11.6 +/- 5.5 pg/ml. Both plasma norepinephrine and renin activity increased in the normal subjects, but failed to increase from higher baselines in patients with congestive heart failure. Thus, plasma arginine vasopressin, like plasma norepinephrine and renin activity, does not increase in response to upright tilt in patients with congestive heart failure. The explanation is not evident but could involve either abnormalities in reflex control of plasma vasopressin in congestive heart failure or in clearance of the hormone during orthostasis.
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PMID:Impaired response of plasma vasopressin to orthostatic stress in patients with congestive heart failure. 635 40

The pathophysiology of heart failure is closely associated with neuroendocrine changes. Activation of these humoral systems apparently serves as a compensatory mechanism for the failing circulation. However, overshoot of such mechanisms may further depress cardiac function by increasing afterload, resulting in a vicious cycle of reflex neuroendocrine activation. Corollary decreases in renal function activate the renin-angiotensin-aldosterone system as well, which further contributes to the cycle of downward-spiralling cardiac function. Many hormonal factors are increased in congestive heart failure. While some influences are vasodilatory, the net effect is marked vasoconstriction. The level of activation of these systems apparently corresponds to the severity of heart failure. Furthermore, elevated levels of these hormones, including norepinephrine, atrial natriuretic factor, plasma renin, and plasma arginine vasopressin, may play a more direct role in worsening heart failure. In fact, elevated catecholamine levels are directly related to prognosis. Catecholamines increase myocardial oxygen demand and are also arrhythmogenic. Oral catecholamines and phosphodiesterase inhibitors, which work by similar mechanisms, have yielded increased mortality rates in heart failure trials. In contrast, mortality rates are reduced in patients treated with angiotensin-converting enzyme inhibitors. Thus, it is clear that neuroendocrine changes are not only a marker of the severity of heart failure, but also directly worsen it. Interventions that antagonize or diminish these neuroendocrine changes apparently benefit patients with heart failure.
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PMID:Neuroendocrine changes in heart failure and their clinical relevance. 758 61

The role of the brain renin-angiotensin system (RAS) in heart failure was examined by administering intracerebroventricular (ICV) infusions of the angiotensin II (ANG II) type 1 (AT1)-receptor antagonist losartan (0.1 followed by 0.5 mg.kg-1.3 h-1) to six concious sheep before (nonpaced) and after induction of heart failure by rapid left ventricular pacing (paced). In both nonpaced and paced states, ICV losartan abolished drinking, induced a significant diuresis (P < 0.05) and anti-natriuresis (P < 0.05), and increased plasma renin activity (P < 0.05) and ANG II (P < 0.01) and aldosterone levels (0.1 > P > 0.05). Plasma arginine vasopressin was suppressed by ICV losartan only in the paced state (P < 0.05). Hemodynamics were not altered by ICV losartan in the nonpaced animals. In the paced state, however, significant reductions in left ventricular systolic, mean arterial, and left atrial pressures were observed (decrements of 13 +/- 7, 12 +/- 5, and 3.4 +/- 0.7 mmHg, respectively, all P < 0.05). In conclusion, ANG II within the brain participates in the regulation of thirst and body electrolyte and fluid homeostasis in normal and heart-failed sheep and appears to play a role in regulating resting hemodynamic status in this model of heart failure.
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PMID:Central angiotensin II AT1-receptor antagonism in normal and heart-failed sheep. 765 6

Endothelins (ET) are a family of peptides with potent biological properties. Endothelial cells produce exclusively ET-1 while other tissues produce ET-2 and ET-3. The production of ET requires an increase in intracellular Ca2+. This increase can be induced by physical chemicals (i.e. hypoxia) or receptor-operated stimuli (i.e. thrombin, angiotensin II, arginine vasopressin, transforming growth factor beta 1, interleukin-1). Most of ET is released abluminally towards vascular smooth muscle and less luminally. The main vascular effect of ET are vasodilation (transient), profound and sustained vasoconstriction as well as proliferation of vascular smooth muscle. These biological effects are mediated by distinct receptors. Three ET receptors have been cloned, i.e. ETA-, ETB- and ETC-receptors. In vascular tissue ETA-receptors are expressed on vascular smooth muscle and responsible for vasoconstriction. ETB-receptors are expressed on endothelium and linked to nitric oxide and/or prostacyclin release. Activation of these receptors explains the transient vasodilation with intraluminal application of ET. Vascular smooth muscle cells can express ETB-receptors which contribute to ET-induced vasoconstriction particularly at lower concentrations. The role of the recently cloned ETC-receptor in the vasculature is still uncertain. ET production is increased (as judged from circulating plasma levels) in vascular disease and atherosclerosis in particular, in myocardial infarction and heart failure, pulmonary hypertension and renal disease. ET production is increased in arterial hypertension remains controversial. Non-peptidic ET antagonists have been developed which either block ETA- receptors or ETA- and ETB-receptors simultaneously. The advantage of ETA-receptors is that they leave the endothelium-dependent vasodilation to ET (via ETB-receptor) intact. However, ETB-mediated contraction remains unaffected by these antagonists. In contrast ETA-/ETB-antagonists fully prevent ET-induced vasoconstriction, however, they also inhibit the endothelial effects of the peptide. ET antagonists interfere with the effects of ET in isolated vascular tissue (including that obtained from humans) as well as in vivo. In humans, ETA as well as ETA-/ETB-antagonists inhibit endothelin-induced vasoconstriction. Hence in summary ET are a family of potent peptides with profound effects in the vasculature. Several studies suggest a role of ET in cardiovascular disease. The newly developed ET-antagonists are potent and selective tools to delineate the (patho-)physiological roles of ET and may become a new class of cardiovascular drugs.
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PMID:Endothelin and endothelin antagonists: pharmacology and clinical implications. 771 86

The understanding of the pathophysiology of heart failure is an emerging science. Although the mortality rate remains high, there has been some improvement in treatment in recent years. What was once thought to be a purely hemodynamic disorder now is understood to be a disease of cellular pathophysiology. The progression of compensated ventricular dysfunction to symptomatic heart failure is marked by the activation of vasoconstrictor hormones. Norepinephrine, renin-angiotensin-aldosterone, and arginine vasopressin are secreted in response to inadequate systemic perfusion. These combine to increase preload and afterload on an already failing heart. Baroreceptor function is attenuated, allowing for the continued sympathoexecitatory state. In addition, local tissue factors mitigate against a return to normal ventricular function by down-regulation of beta receptors, stimulation of local vasoconstrictor hormone secretion, and promotion of growth. Patients in intensive care units with chronic heart failure are best managed with an understanding of how their altered physiology affects their clinical presentation.
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PMID:Pathophysiology of heart failure: neuroendocrine response. 771 45


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