Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in plasma level of arginine vasopressin (AVP), arterial pressure, and urine flow were studied before, during and after cardiopulmonary bypass (CPB) in 11 patients with congenital heart disease. Anesthesia was induced with thiopental sodium (3-5 mg/kg) and was maintained with enflurane (1.0-1.5%), 50% N2O in O2 and morphine (0.5 mg/kg). Concentration of plasma AVP increased slightly from 3.8 +/- 1.5 pg/ml after induction and increased 3-fold after sternotomy. Plasma AVP level increased to 132 +/- 26 pg/ml and 218 +/- 54 pg/ml after 5 and 60 min on CPB, respectively. When the circulation returned to normal, plasma AVP level decreased gradually but was still significantly higher at 24 hr (13.4 +/- 2.5 pg/ml). Marked osmolar diuresis was induced with mannitol in the priming solution used during the CPB: increases in urine flow, Na excretion and osmolar clearance. Possible mechanisms of marked increase in AVP release and differences of AVP responses during CPB reported by other investigators are discussed.
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PMID:Responses of vasopressin release in patients with cardiopulmonary bypass anesthetized with enflurane and morphine. 259 63

Three women with neurohypophyseal diabetes insipidus, treated for prolonged periods, including pregnancy, with L-deamino-8-d-arginine vasopressin, gave birth in our hospital. Two of the infants had severe congenital heart disease, one of which was associated with trisomy 21. The third baby, born prematurely, presented with mild intrauterine growth retardation; at the age of 21 months, the boy had severe failure to thrive, hypotonia, and motor retardation. These three cases raise doubts as to the safety of diabetes insipidus or its treatment in pregnancy.
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PMID:L-deamino-8-d-arginine vasopressin treatment in pregnancy and neonatal outcome. A report of three cases. 371 35

To examine the contributions of cardiopulmonary and sinoaortic baroreceptors to the nonosmotic release of arginine vasopressin (AVP) in normal humans, we subjected nine individuals without evidence of hypertension or heart disease to graded, lower body negative pressure (LBNP). We also studied the effects of this maneuver on sympathetic nervous system activity using plasma norepinephrine (NE) as an index. Heart rate (HR), mean arterial pressure (MAP), pulse pressure (PP), and central venous pressure (CVP) were measured in the control state and during two consecutive levels of increasingly intense LBNP. At each stage blood was sampled for AVP and NE. AVP was analyzed by radioimmunoassay, NE by a radioenzymatic method. During the first level of LBNP, CVP decreased with no change in HR, MAP, or PP. NE increased from 147 +/- 47 to 212 +/- 53 (SD) pg/ml, P less than 0.01, whereas AVP (5.0 +/- 1.0 pg/ml) did not change. With increased suction CVP fell further, HR increased, and PP narrowed, but MAP did not change. NE further increased to 291 +/- 58 pg/ml (P less than 0.01), but AVP still did not change significantly. One subject became markedly hypotensive, and his AVP increased from 2.6 to 81 pg/ml. A fall in CVP that results in sympathetic activation presumably via cardiopulmonary receptors does not therefore increase AVP levels; a further fall in CVP that leads to modest unloading of the sinoaortic baroreceptor and further increased sympathetic activity also fails to stimulate AVP. Hypotension, however, is accompanied by a rapid and profound increase in circulating AVP.
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PMID:Response of vasopressin and norepinephrine to lower body negative pressure in humans. 714 50

We studied the changes in the plasma concentration of atrial natriuretic factor (ANF) and the urinary excretion of ANF, arginine vasopressin (AVP) and catecholamines in 22 children with congenital heart disease, divided into two groups. Group 1 included 11 children with congestive heart failure (CHF), treated with digitalis and diuretics. Group 2 included 11 children without CHF and without medical treatment. Each group was compared with a control group of 15 healthy, age-matched children. The plasma concentration of ANF was raised in both groups, but it was significantly higher in group 1 (235.5 +/- 82.9 pg/ml), compared to group 2 (48.4 +/- 29.4 pg/ml, P < 0.002). Urinary excretion of ANF was measurable in both groups and higher in group 1 (185.9 +/- 116.2 pg/kg per h) than in group 2 (48.5 +/- 30.7 pg/kg per h), but not significantly so. Urinary excretion of AVP and catecholamines was not different in children with congenital heart disease and healthy children. Twenty-four hours after surgery, plasma ANF diminished in group 1 (from 235.5 +/- 82.9 to 93.4 +/- 53.8 pg/ml, P < 0.003), but did not change in group 2. The urinary excretion of ANF was unchanged in both groups. In contrast, urinary excretion of AVP and catecholamines rose significantly in both groups. These data show that plasma ANF is increased in children with congenital heart disease, even in the absence of CHF. The measurement of urinary ANF is less reliable than a plasma assay. The postoperative increases in AVP and catecholamine urinary excretions could be responsible for the vasoconstriction and water retention typical of the postoperative period.
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PMID:Plasma levels of atrial natriuretic factor (ANF) and urinary excretion of ANF, arginine vasopressin and catecholamines in children with congenital heart disease: effect of cardiac surgery. 826 94

We have reported that the plasma endothelin-1 (ET-1) level is significantly increased by exercise in healthy athletes and that it is elevated in the circulation of the non-working leg but not the working leg, suggesting that ET-1 plays an important role in redistribution of blood during exercise. This study was designed to compare alterations of neurohumoral substances by exercise in normal subjects and patients with heart disease. Study patients comprised three groups: eight patients with congestive heart failure (CHF) due to Ebstein's anomaly or single-ventricle heart after Fontan operation; six patients with complete transposition of the great arteries (TGA) after an anatomic surgical correction who may be candidates for ischemic heart disease; and five age-matched normal subjects. All patients were in New York Heart Association functional class I. All subjects performed symptom-limited treadmill exercise. It is suggested that patients with CHF or TGA have a manifest or latent exercise intolerance, respectively. In failed to increase plasma ET-1 level, although it caused a greater increase in norepinephrine, angiotensin II, and arginine vasopressin than in the controls. Exercise also caused a delay in the increased response of plasma ET-1 levels in patients with TGA after an anatomic surgical repair. On the other hand, plasma brain natriuretic peptide (BNP) level was augmented by exercise in patients with CHF and patients with TGA but not in the controls. The present results suggest that an increase in ET-1 production during exercise is absent in patients with heart disease. The mechanisms of inhibition of ET-1 production during exercise in patients with heart disease remain to be elucidated. However, the present study suggests that ET-1 plays an important role in redistribution of blood during exercise, and proposes the possibility that failure of an increase in ET-1 production results in exercise intolerance in patients with heart disease.
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PMID:Abnormal neurohumoral responses to exercise in patients with heart disease: inhibition of an increase in endothelin-1 production during exercise. 959 98

Traditionally, the pathophysiology of heart failure was viewed as a derangement in hemodynamic factors. Impairment in cardiac function resulted in decreased cardiac output and end-organ hypoperfusion triggering compensatory increases in heart rate, blood pressure and cardiac contractility. While initially beneficial, these mechanisms placed additional stress on the failing heart. Unfortunately, pharmacologic therapies that restored hemodynamic balance failed to halt disease progression. The activation of neurohormonal responses, including those of the renin-angiotensin-aldosterone system, the sympathetic nervous system and the arginine vasopressin system, has been implicated in the progression of heart disease. In acute heart failure, their effects help to restore cardiovascular homeostasis. However, the chronic stimulation of these systems eventually leads to worsening left ventricular function. Drug treatments that activate neurohormonal systems may have long-term clinically deleterious outcomes, and therefore new pharmacological therapies for cardiovascular disease must take into account the interaction between neurohormonal activation and hemodynamic factors.
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PMID:Neurohormonal activation in the treatment of congestive heart failure: basis for new treatments? 969 63

Chronic obstructive pulmonary disease (COPD) often leads to massive oedema and the development of what is usually called cor pulmonale. The mechanisms by which patients with COPD retain salt and water are not completely understood. Several abnormalities have been found including reduced renal blood flow with relatively preserved glomerular filtration rate and elevated levels of renin, aldosterone, arginine vasopressin and atrial natriuretic peptide. Generally, these abnormalities worsen with the severity of COPD and are most marked during the oedematous phases. Cardiac output is remarkably normal, suggesting that "cor pulmonale" is not primarily a cardiac disorder but rather a condition of volume overload due to activation of sodium-retaining mechanisms. The stimulus for this activation could be underfilling of the arterial system (reduced effective circulating volume) secondary to a fall in total peripheral vascular resistance. The latter is caused by hypercapnia-induced dilation of the precapillary sphincters. Apparently, the massive sodium retention by the kidney is not able to restore the circulating volume and a vicious cycle ensues ultimately leading to a clinical picture which resembles right-sided heart failure. Predictably, only blockade of the effects of carbon dioxide at the level of the precapillary sphincters would be able to halt this process.
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PMID:Fluid homeostasis in chronic obstructive lung disease. 1462 Nov 5

Heart failure is one of the most common, costly, disabling and growing diseases (McMurray and Pfeffer in Lancet 365(9474):1877-1889, 2005). Hyponatremia, conventionally defined as a serum-sodium concentration equal or less than 135 mmol/l (American Heart Association in Heart disease and stroke statistics--2007 update. American Heart Association, Dallas, 2007; Stewart et al. in Eur J Heart Fail 4:361-371, 2002), is a common phenomenon in patients with heart failure, with an incidence of 20-25% (Krumholz et al. in Arch Intern Med 157:e99-e104, 1997; Rosamond et al. in Circulation 117(4):e25-e146, 2008; Adrogue and Madias in N Engl J Med 342:1581-1589, 2000) and seems to be of prognostic importance in patients with heart failure (Luca et al. in Am J Cardiol 96:19L-23L, 2005; Gheorghiade et al. in Eur Heart J 28:980-988, 2007; Gheorghiade et al. in Arch Intern Med 167:1998-2005, 2007). So far treatment strategies have been limited and burdened by side effects. The development of hyponatremia in the setting of heart failure is related to the arginine vasopressin (AVP) dysregulation. Thus, AVP receptor antagonists are a promising approach to treatment. However, several questions remain: whether there is a cause-and-effect mechanism, if the correction of hyponatremia improves outcomes, and defining the specific cut-off level of serum-sodium that should be used to define hyponatremia. In this review, we aim to summarize the literature on hyponatremia in patients with heart failure within several aspects: incidence in clinical trials and registries, prognostic value, underlying mechanisms, therapeutic options, and possible future perspectives.
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PMID:Significance of hyponatremia in heart failure. 2083 81

The hypothalamic-pituitary-adrenal axis is activated in response to stress. One of the activated hypothalamic hormones is arginine vasopressin, a hormone involved in hemodynamics and osmoregulation. Copeptin, the C-terminal part of the arginine vasopressin precursor peptide, is a sensitive and stable surrogate marker for arginine vasopressin release. Measurement of copeptin levels has been shown to be useful in a variety of clinical scenarios, particularly as a prognostic marker in patients with acute diseases such as lower respiratory tract infection, heart disease and stroke. The measurement of copeptin levels may provide crucial information for risk stratification in a variety of clinical situations. As such, the emergency department appears to be the ideal setting for its potential use. This review summarizes the recent progress towards determining the prognostic and diagnostic value of copeptin in the emergency department.
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PMID:The role of copeptin as a diagnostic and prognostic biomarker for risk stratification in the emergency department. 2226 20