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

The hemodynamic and hormonal changes produced by adriamycin-induced cardiomyopathic congestive heart failure in rabbits were studied. Adriamycin cardiomyopathy in rabbits led to ventricular dilatation, pleural and pericardial effusions, hepatic congestion, and ascites. These pathological changes were associated with the maintenance of a normal blood pressure but a lowered cardiac output and increased total peripheral resistance. Plasma renin activity and plasma norepinephrine were increased twofold in rabbits with congestive cardiac failure. However, plasma vasopressin and osmolality were normal, whereas an increased vascular sensitivity to the infusion of exogenous vasopressin was demonstrated. Despite the normal levels of plasma vasopressin, administration of a specific vascular vasopressin antagonist led to a fall in blood pressure, a significant increase in cardiac output, and a decrease in total peripheral resistance. No such hemodynamic changes occurred on infusing normal rabbits with the vascular vasopressin antagonist, nor did any significant hemodynamic changes occur on injecting vehicle in rabbits with heart failure. These results suggest that in adriamycin-induced cardiomyopathic heart failure in rabbits, there is activation of the renin-angiotensin system and the sympathetic nervous system together with an increased sensitivity to vasopressin. These three hormonal systems help to maintain blood pressure by increasing total peripheral resistance in this experimental model of heart failure.
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PMID:Role of vasopressin in experimental congestive cardiac failure. 243 82

Atrial natriuretic peptides (ANP) exert vasodilating and natriuretic actions. The present study was undertaken to test the effect of low dose infusions of synthetic ANP on hemodynamic and humoral variables of patients with severe heart failure. Eight patients, aged 26 to 71 years, with severe congestive heart failure due to ischemic heart disease or idiopathic dilated cardiomyopathy were included in the study. Synthetic human (3-28) ANP was infused at doses ranging from 0.5 to 2 micrograms/min for up to 3 h. Pulmonary capillary wedge pressure fell from 24 +/- 1 to 16 +/- 2 mm Hg (mean +/- SEM) (p less than 0.01) and cardiac index tended to rise from 2 +/- 0.2 to 2.3 +/- 0.2 L/min/m2 (NS), while blood pressure and heart rate did not change. One patient experienced a marked drop in pulmonary capillary wedge and arterial blood pressure that necessitated the administration of saline. ANP infusion did not alter plasma renin activity or plasma aldosterone, norepinephrine, or vasopressin levels. It decreased plasma epinephrine levels from 0.472 +/- 0.077 to 0.267 +/- 0.024 nmol/L (p less than 0.05). Plasma ANP levels were markedly elevated in all patients before initiating the infusion. They had no predictive value for the hemodynamic response to exogenous ANP. No correlation was observed between the hemodynamic effects of ANP and those induced by the subsequently administered converting enzyme inhibitor captopril, which seemed to improve cardiac function more consistently.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Infusion of atrial natriuretic peptide to patients with congestive heart failure. 246 56

Patients with chronic heart failure (CHF) have increased plasma levels of the antidiuretic hormone arginine vasopressin (AVP). The stimulus for increased AVP secretion is unknown, but appears to involve a nonosmotic drive which alters normal osmoregulatory mechanisms. Centrally acting alpha 2-adrenergic agonists suppress AVP secretion in experimental animals. To examine the hypothesis that such effects might be apparent on the chronically elevated AVP levels in patients with CHF, we measured AVP, heart rate (HR), mean arterial pressure (MAP), and plasma norepinephrine (NE) after 4 mg oral guanabenz in nine patients with this disease. Plasma NE decreased from 513 +/- 131 to a minimum of 371 +/- 117 pg/ml (p less than 0.02) 5 h postdrug. HR decreased from 80 +/- 9.3 to 74 +/- 10 beats/min (p less than 0.05) and MAP decreased from 88 +/- 8.5 to 83 +/- 10 mm Hg (p less than 0.05). Plasma AVP, however, did not change from baseline levels of 5.6 +/- 1.6 pg/ml. Serum osmolality was also constant. These data do not support a possible role for acute increases of alpha 2-adrenergic activity in suppressing the increased plasma AVP levels of CHF, at least under basal conditions at constant osmolality.
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PMID:Alpha 2-adrenergic stimulation and vasopressin in congestive heart failure. 247 22

The characteristics of norepinephrine and epinephrine as well as plasma renin activity, angiotensin II, aldosterone, vasopressin, and atrial natriuretic factor (ANF) were examined in 64 patients (mean age of 52 +/- 16 years) with dilated cardiomyopathy. The findings were grouped according to the NYHA classification and compared with a normal cohort of 38 patients (mean age of 42 +/- 10 years). Furthermore, the influence of different cardioactive substances used in the treatment of cardiac failure was analyzed in more detail. Patients in NYHA class II already demonstrated an increased activity of the sympathicoadrenal, renin-angiotensin-aldosterone system (RAAS), vasopressin, and ANF system. The highest values were found in patients of NYHA class IV. In these patients, norepinephrine was enhanced by a factor of 7, epinephrine by a factor of 2, plasma renin activity by a factor of 7, angiotensin II by a factor of 2.5, aldosterone by a factor of 5, vasopressin by a factor of 1.5, and ANF by a factor of 4 compared with those in normal subjects. The highest correlation coefficient was found for norepinephrine (r = 0.84). The acute application of 1-2 mg/kg of body weight of enoximone in patients with dilated cardiomyopathy (n = 15) resulted only in a significant lowering of the atrial natriuretic factor as an indicator for drug-induced unloading effects (venous pooling). All the parameters showed only a tendency; in none could statistical significance be established. Application of 0.75 mg/kg of body weight of enoximone i.v. in patients with coronary artery disease (n = 17) has no direct influence either on the sympathoadrenal, the ANF, or the prostaglandin systems. It could be demonstrated that the mode of medical treatment influences the parameters of vasoconstrictor systems in different ways.
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PMID:The influence of various degrees of cardiac failure, chronic medical treatment, and acute additional enoximone application on the parameters of the vasopressor system. 248 Apr 85

Because the syndrome of inappropriate antidiuretic hormone (SIADH) is a state of disturbed body fluid volume regulation and altered sodium balance we sought to determine if recently described volume regulatory factors were stimulated in SIADH. We measured atrial natriuretic peptide (ANP), endogenous digitalis-like natriuretic factor (EDNF) and urinary free dopamine in SIADH (n = 27). We also determined fractional clearance of lithium (FCLi). The data obtained in SIADH were compared with similar measurements performed in sodium retaining hyponatremias, such as those of heart failure (n = 26), liver cirrhosis (n = 19) and volume contraction (n = 28). We observed: ANP was 19.5 +/- 2.7 fM/ml in SIADH; it was significantly lower than ANP in cardiac failure, but no different from ANP in volume contraction. Urinary free dopamine was 2.2 +/- 0.8 microM/24 h in SIADH; this was significantly higher than in volume contraction and liver cirrhosis. EDNF (259 +/- 42 nM/24 h) and FCLi (21.4 +/- 2%) were both numerically higher in SIADH than in other hyponatremic disorders; however, the differences did not achieve significance. In conclusion, our observations did not establish a specific role of ANP in chronic stable SIADH. As to the importance of EDNF, dopamine and proximal tubular fluid reabsorption (FCLi) additional work using acute volume changes may demonstrate their participation in the renal sodium handling of SIADH more clearly than our study did.
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PMID:Natriuretic factors and lithium clearance in patients with the syndrome of inappropriate antidiuretic hormone (SIADH) 250 58

The aim of this paper was to study plasma atrial natriuretic factor, renin activity, aldosterone and antidiuretic hormone in low-output heart failure syndromes such as cardiogenic shock, hypovolemic shock and hypotension with bradycardia syndrome. A total of 30 patients were investigated: 10 with cardiogenic shock due to acute myocardial infarction of the anterior wall (systolic and diastolic blood pressure 56.0 +/- 3.7/40.5 +/- 2.0 mmHg; heart rate 119.7 +/- 1.2 beats/min; central venous pressure 16.2 +/- 0.6 cmH2O) (I group), 10 with hypovolemic shock induced by melena in peptic ulcer (systolic and diastolic blood pressure 74.5 +/- 1.5/57.5 +/- 1.7 mmHg; heart rate 111.0 +/- 1.4; central venous pressure 6.3 +/- 0.5 cmH2O) (II group), 10 with hypotension with bradycardia syndrome which occurred in patients during acute myocardial infarction of the inferior wall (systolic and diastolic blood pressure 71.9 +/- 2.0/58.0 +/- 2.6 mmHg; heart rate 52.0 +/- 2.2 beats/min; central venous pressure 4.6 +/- 0.4 cmH2O) (III group). Plasma atrial natriuretic factor values were measured using radioimmunoassay after chromatographic pre-extraction; plasma renin activity, aldosterone and antidiuretic hormone values were calculated using radioimmunoassay. Circulating atrial natriuretic factor was significantly (p less than 0.01) higher in patients with cardiogenic shock (102.4 +/- 7.4 pg/ml) than in healthy volunteers (8.4 +/- 0.3 pg/ml). In the former there was a positive correlation between atrial natriuretic factor and central venous pressure values. Atrial natriuretic factor and central venous pressure values in the IInd and IIIrd groups of patients were in the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Atrial natriuretic factor in cardiogenic shock, in hypovolemic shock and in the bradycardia-hypotension syndrome following acute myocardial infarction]. 253 Jan 27

Congestive cardiac failure is a syndrome in which a decrease of cardiac output triggers a series of neuro-humoral compensatory mechanisms in part involving the kidney. In this response, dysfunction of atrial volume receptors as well as disturbances of the autonomic nervous system have recently been demonstrated and are held responsible for excessive stimulation of angiotensin II, followed by adverse regulatory effects. Renal hemodynamic compensation for heart failure primarily involves constriction of efferent arterioles thereby defending glomerular filtration. In this setting, the occurrence of prerenal insufficiency is indicative of a far advanced reduction in renal blood flow. Apparent diuretic resistance in the treatment of heart failure is usually caused by iatrogenic vascular compromise or by the use of a single diuretic rather than an appropriate combination. Hyponatremia, vasopressin stimulation and elevation of plasma N-epinephrine concentration have been found to be the most reliable indicators of a poor prognosis of heart failure. Atrial natriuretic peptide is stimulated in proportion to the degree of atrial distension in heart failure, however its intrarenal effects are markedly blunted or may even be absent in this particular disease.
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PMID:[Kidney function in heart failure]. 253 Mar 91

The non-osmotic stimulation of release of arginine vasopressin (AVP) seems to be the main determinant of the impaired water excretion and hyponatraemia in patients with cardiac failure. This non-osmotic stimulation of AVP release could be secondary to a decrease in stroke volume to which the ventricular receptors respond by decreasing the vagal afferent input to the hypothalamus via the mid-brain. Improvement of cardiac stroke volume would then decrease AVP release and improve water excretion. In cardiac failure, the non-osmotic stimulation of AVP release is not clearly modulated by the renin-angiotensin system or by the atrial natriuretic peptide plasma concentration. Nevertheless, physiological concentrations of atrial natriuretic peptide could inhibit the renal epithelial water transport at the collecting duct level. Water-loading and osmotic-loading experiments in patients with cardiac failure indicated that the release of AVP is still under osmotic control and favoured the concept that volume depletion in general and cardiac failure in particular may lower the osmotic threshold and increase the osmotic sensitivity to vasopressin release. Experiments using a specific vasopressin antagonist rarely indicated a vasoconstrictor role for endogenous AVP in either experimental or clinical cardiac failure. Intrarenal factors also contributed to the impaired water excretion observed in patients with cardiac failure: increased central sympathetic efferent discharge and stimulation of the renin-angiotensin-aldosterone system would be expected as a consequence of the decreased effective arterial blood volume. These effects could then decrease maximal reabsorption of solute further impairing the ability of the kidney to excrete free water. The impaired water excretion is correlated with the severity of the cardiac deterioration and thus has prognostic implications.
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PMID:Water disturbances in cardiac failure. 253 70

Alterations in the vasopressor system found in cardiac failure are part of compensatory measures that may modify pharmacologic-therapeutic response. Therefore, in 64 patients with dilated cardiomyopathy, we investigated its enhanced activity in different clinical stages of the disease as compared to normal controls. Patients in NYHA class II (n = 20) demonstrated increased activity of the sympathico-adrenal, renin-angiotensin-aldosterone, vasopressin, and atrial natriuretic factor systems, while maximum values were found in patients of NYHA class IV (n = 24). In these patients, noradrenaline was enhanced by a factor of 7, adrenaline by a factor of 2, plasma-renin-activity by a factor of 7, angiotensin II by a factor of 2.5, aldosterone by a factor of 5, vasopressin by a factor of 1.5, and ANF by a factor of 4 as compared to normal controls. Clinical NYHA classes correlated to a certain degree with the various plasma hormones. Patients treated with an aldosterone inhibitor in addition to digitalis and diuretics revealed significantly higher values for aldosterone, vasopressin, and angiotensin II as compared to those who received digitalis and diuretics alone. The addition of ACE-inhibitor therapy resulted in a decrease of angiotensin II, aldosterone, and vasopressin. Plasma catecholamines and ANF, however, did not change under the influence of cardiac medication. Diuretic treatment in NYHA class II patients reduced plasma volumes (p less than 0.01). Plasma volume in NYHA class IV patients only was found to be higher than in normal controls. Thus, analysis of the neurohumoral system can aid both in the identification of the clinical degree of dilated cardiomyopathy and in its optimal therapy.
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PMID:The vasopressor system in patients with heart failure due to idiopathic dilated cardiomyopathy--influence of the clinical stage of disease and of chronic drug treatment. 253 2

The objective of this study was to determine the effects of transient aortic valve occlusion (balloon valvuloplasty) on vasoactive hormones in patients with heart failure. Plasma atrial natriuretic peptide, vasopressin, aldosterone, adrenocorticotropic hormone (ACTH), and plasma renin activity were measured before, immediately after, and 30 minutes and 18 to 24 hours following balloon inflation in 18 patients. Mean right atrial and pulmonary wedge pressures were 6 and 18 mm Hg before inflations, respectively, and were unchanged after balloon inflations (5 and 13 mm Hg, respectively). Systemic systolic/diastolic pressures were 139 +/- 8/65 +/- 4 mm Hg before occlusion, decreased to 47 +/- 5/34 +/- 3 mm Hg during occlusion, and returned to baseline after occlusions. Baseline atrial natriuretic peptide levels were 267 +/- 43 pg/ml and increased to 513 +/- 71 pg/ml after balloon inflations. Vasopressin levels before occlusion were 9.1 +/- 2.2 pg/ml and increased to 21.4 +/- 4.8 pg/ml after balloon inflations. Plasma renin activity was 5.4 +/- 1.4 ng/ml/hr before inflations and was not significantly changed after balloon inflations. No clinically significant changes in plasma sodium, potassium, creatinine, and osmolality were observed after the procedure. Aldosterone increased from 23 +/- 4 to 40 +/- 7 ng/dl 10 minutes after the last inflation. Plasma ACTH measured in seven patients with increased aldosterone was 28 +/- 8 pg/ml before and increased to 295 +/- 157 pg/ml 10 minutes after balloon inflations. The increases in natriuretic peptide and vasopressin were likely due to elevated intracardiac and decreased arterial pressures, respectively; they persisted in spite of no clinically significant changes in filling pressures 12 to 24 hours after the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stimulation of atrial natriuretic peptide and vasopressin during percutaneous transluminal aortic valvuloplasty. 254 14


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