Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although glucagon exerts positive inotropic effects in patients with no or mild impairment of cardiac function, similar effects are not consistently observed in patients with chronic heart failure. Accordingly, the inotropic effects of glucagon on papillary muscles from normal cats and cats in which right ventricular failure had been produced for 4-145 days by pulmonary artery banding were compared. At the peak of the concentration-response curve, glucagon increased peak isometric tension (T) in normal muscles from 4.4+/-0.4 to 6.6+/-0.5 g/mm(2) (P <0.001), and maximum rate of tension development (dT/dt) from 16.9+/-0.9 to 25.1+/-1.6 g/sec per mm(2) (P < 0.001). In contrast, glucagon produced no significant increases in T or dT/dt in failure muscles. The percentage increases in T and dT/dt caused by norepinephrine were the same in muscles from normal and failing hearts. Since the cardiac effects of glucagon and norepinephrine may be mediated by adenyl cyclase, responsiveness of adenyl cyclase was determined in particulate fractions of the right ventricle. Glucagon activated adenyl cyclase in normal, but had no effect in failure preparations. Norepinephrine-induced activation of adenyl cyclase, however, was unaltered by failure. Thus, in contrast to norepinephrine, glucagon loses the capacity to augment myocardial contractility and activate adenyl cyclase in hearts derived from cats in chronic failure.
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PMID:Effects of experimental heart failure on the capacity of glucagon to augment myocardial contractility and activate adenyl cyclase. 544 51

This study was designed to investigate the changes in the beta adrenergic system during the induction of cobalt cardiomyopathy in dogs. Cobalt sulphate, at a dose of 5 mg X kg-1 X day-1 was administered intravenously with a low protein, low thiamine diet to 13 dogs. The percentage change of the left ventricular minor axis with systole by echocardiogram (% delta D) and dP/dtmax were used to monitor left ventricular function. Noradrenaline (NA) was measured in 24 h urine samples. Left ventricular (LV) free wall biopsies were assayed for noradrenaline (LV-NA), cyclic AMP, cyclic GMP and dopamine beta hydroxylase (LV-DBH). Lymphocytes were assayed for beta-receptor density. All dogs were studied at baseline and seven were studied after a midpoint cumulative dose of 60 to 90 mg X kg-1 of cobalt; the remaining six dogs were studied when they were in heart failure and had received more than 110 mg X kg-1. During the induction of heart failure the heart rate rose from 112 +/- 6 (means +/- SE) at baseline to 154 +/- 9 at the midpoint and 153 +/- 9 (both P less than 0.05) at the final measurement while the % delta D fell from 35 +/- 2% to 31 +/- 3% and 23 +/- 2% (P less than 0.05) and dP/dt fell from 333 +/- 40 kPa X s-1 at baseline to 254 +/- 46 kPa X s-1 (P less than 0.05) and 207 +/- 33 kPa X s-1 (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The evolution of beta-adrenergic dysfunction during the induction of canine cobalt cardiomyopathy. 631 98

The relationships between hemodynamic state and plasma components of the renin-angiotensin and adrenergic nervous systems were studied in 42 patients admitted to an intensive care unit with acute heart failure. Patients were allocated to four subsets according to cardiac output and pulmonary wedge pressure. Plasma renin activity and angiotensin II were abnormally high in most patients with cardiac output less than or equal to 3.81 X min-1 and pulmonary wedge pressure greater than or equal to 18 mm Hg in contrast with values of patients of the 3 other subsets, which overlapped the normal range. On the other hand, plasma catecholamines were abnormally high in most patients. Angiotensin II was positively correlated with pulmonary wedge pressure, urea and catecholamines and negatively correlated with cardiac output and natremia. Norepinephrine was uncorrelated with hemodynamic parameters but epinephrine was negatively correlated with cardiac output. A discriminant linear function was calculated for prognosis of survival: cardiac output was the most important factor. The rise of angiotensin II and epinephrine were not unfavorable factors if their correlations with other factors (e.g. cardiac output and urea) were taken into account.
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PMID:Relationships between plasma epinephrine, norepinephrine, dopamine and angiotensin II concentrations, renin activity, hemodynamic state and prognosis in acute heart failure. 637 23

Hemodynamics, plasma norepinephrine, and plasma renin activity were measured at supine rest in 106 patients (83 men and 23 women) with moderate to severe congestive heart failure. During follow-up lasting 1 to 62 months, 60 patients died (57 per cent); 47 per cent of the deaths were sudden, and 45 per cent were related to progressive heart failure. Statistically unrelated to the risk of mortality were cause of disease (60 patients had coronary disease, and 46 had cardiomyopathy), age (mean, 54.8 years), cardiac index (mean, 2.11 liters per minute per square meter of body-surface area), pulmonary wedge pressure (mean, 24.5 mm Hg), and mean arterial pressure (mean, 83.2 mm Hg). A multivariate analysis of the five significant univariate prognosticators--heart rate (mean, 84.4 beats per minute), plasma renin activity (mean, 15.4 ng per milliliter per hour), plasma norepinephrine (mean, 700 pg per milliliter), serum sodium (mean, 135.7 mmol per liter), and stroke-work index (mean, 21.0 g-meters per square meter)--found only plasma norepinephrine to be independently (P = 0.002) related to the subsequent risk of mortality. Norepinephrine was also higher in patients who died from progressive heart failure than in those who died suddenly. These data suggest that a single resting venous blood sample showing the plasma norepinephrine concentration provides a better guide to prognosis than other commonly measured indexes of cardiac performance.
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PMID:Plasma norepinephrine as a guide to prognosis in patients with chronic congestive heart failure. 638 11

A high performance liquid chromatographic method was used to determine myocardial norepinephrine and epinephrine concentrations in 66 biopsy specimens obtained from the right or left ventricle during routine diagnostic cardiac catheterization of 45 patients with dilated (congestive) or hypertrophic cardiomyopathy, or with heart disease other than cardiomyopathy, such as acute perimyocarditis, postmyocarditis and constrictive pericarditis. The validity of catecholamine determination in a 2 to 6 mg biopsy specimen to assess overall ventricular myocardial catecholamines was demonstrated. Norepinephrine concentrations in the myocardium were inversely correlated with the grade of hypertrophy in patients with congestive cardiomyopathy or heart disease other than cardiomyopathy, but not in patients with hypertrophic cardiomyopathy. The fact that the myocardial norepinephrine concentration was always lower in the left than in the right ventricle of the same patient may be explained by the simple dilution of sympathetic nerve endings in the left ventricle. There were some cases of hypertrophic cardiomyopathy in which the concentration of myocardial norepinephrine was exceptionally high, although its mean value was not significantly higher than that in patients with other types of heart disease who served as a control group without cardiomyopathy. Some patients with dilated cardiomyopathy had lower levels of myocardial norepinephrine than would be expected for the degree of interstitial fibrosis and the severity of heart failure. The mean plasma norepinephrine and epinephrine levels were significantly elevated in patients with dilated cardiomyopathy.
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PMID:Myocardial catecholamines in hypertrophic and dilated (congestive) cardiomyopathy: a biopsy study. 668 49

In a postmortem study of 8 uremic patients (mean age 63.0), the concentration of 23 trace elements was determined in heart tissue with neutron activation analysis. The concentration was significantly increased in 10 elements - e.g. Co (p less than 0.001), As, Br, Ce, La, Sb, Sc (p less than 0.01), Fe, K and P (p less than 0.05) - compared to a control group of non-uremic individuals. As some of these elements are cardiotoxic, the results support our opinion that an excess of certain trace elements, cobalt in particular, may be etiological agents of importance in uremic heart failure.
Nephron 1983
PMID:The role of trace elements in uremic heart failure. 686 79

Vasodilator drugs produce tachycardia and an increase in circulating plasma norepinephrine in normal subjects. In contrast, heart rate does not change when the same drugs are given to patients with congestive heart failure. To assess if this difference could be related to a different reflex activation of the sympathetic nervous system, the response of plasma norepinephrine to nitroprusside infusion and to head-up tilt was studied in 5 normal subjects and in 46 patients with chronic congestive heart failure. Norepinephrine and heart rate increased significantly during both stimuli in normal subjects but were unchanged during nitroprusside infusion for the entire group of patients with heart failure, with considerable variability in individual responses. In 21 patients (Group I) norepinephrine increased during nitroprusside infusion, while in the remaining 25 (Group II) norepinephrine decreased. The hemodynamic response to nitroprusside was similar in the two groups, thus suggesting that the different changes in plasma norepinephrine could not be explained on the basis of a different hemodynamic response to the drug. Plasma norepinephrine also did not change significantly in Group II during tilt, although the decrease in intracardiac pressure and the increase in peripheral resistance were similar to those in Group I who increased norepinephrine normally by 56%. These data indicate that a subset of patients with severe ventricular dysfunction have an abnormal humoral, reflex sympathetic response to changes in arterial or intracardiac pressure, or both. The higher mortality in Group II suggests that this alteration in the sympathetic response may be a marker of the severity and prognosis of heart failure.
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PMID:Abnormal neurohumoral response to nitroprusside infusion in congestive heart failure. 687 5

Changes in endocrine activity in response to tilting of the body were studied in 16 in-patients with various degrees of chronic congestive heart failure and one healthy subject. Norepinephrine and epinephrine excretion, plasma renin activity and plasma cortisol concentration were determined first in recumbency and then during 45 degree head-up tilting. The subjects were divided into three groups depending on the severity of heart failure. In recumbency urinary norepinephrine averaged 31.6 (standard deviation 12.7) ng/min in group 1 (controls), 54.9 +/- 25.3 ng/min in group 2 (NYHA class II--III) and 79.5 ng/min in group 3 (NYHA class IV). Thus the level of urinary norepinephrine increased with the degree of heart failure. In recumbency epinephrine excretion and plasma cortisol concentration were not different among three groups. Plasma renin activity was elevated in group 3. There was a significant positive correlation between the changes in plasma renin activity and epinephrine secretion (r = 0.67, p less than 0.01). The present study revealed that patients with slight to moderate congestive heart failure have a normal endocrine response to tilting while those in severe failure have only a slight response. It is probable that the augmented sympathetic nerve activity and increased circulating blood volume, already present in severe failure, allow for less hemodynamic change upon tilting.
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PMID:Role of endocrine factors in chronic congestive heart failure, with emphasis on catecholamines. 698 19

The interaction of cardiac function and sympathetic tone in severe chronic heart failure was evaluated in 24 patients by assessing the cardiac index/plasma norepinephrine relationship. Potential changes were assessed during first-dose and long-term captopril therapy including sympathetic responsiveness to the gravitational stress of head-up tilt. Because cardiac index and norepinephrine levels demonstrated a significant inverse correlation (r = -0.640, p less than 0.001). Norepinephrine decreased from 803 +/- 116 to 635 +/- 76 pg/ml following first-dose captopril therapy (p less than 0.02), with overall hemodynamic improvement. However significant first-dose correlations were not observed. During long-term therapy, norepinephrine decreased from 694 +/- 118 to 457 +/- 106 pg/ml, associated with improvement of symptoms and exercise tolerance. The extent of cardiac index increase was matched by norepinephrine reduction, so that their correlation was maintained (r = -0.540, p less than 0.02). First-dose and long-term therapy were associated with improved responsiveness of sympathetic tone to the reduction of cardiac index induced by the gravitational stress of tilt. In summary, sympathetic tone was increased in severe heart failure, correlating inversely with cardiac function. Although there was improvement of cardiac function with first-dose captopril therapy, significant correlations of supine improvement with reduction of sympathetic tone were noted primarily with long-term therapy. Responsiveness of sympathetic tone to the stress of tilt however, was evident during first-dose and long-term therapy.
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PMID:Sympathetic responsiveness and plasma norepinephrine during therapy of chronic congestive heart failure with captopril. 704 20

The high blood flow rate/gram of kidney tissue supplies mainly the renal cortex. The net effect of the interaction of the renin-angiotensin system, the kallikrein-kinin system and prostaglandins is to autoregulate renal blood flow within a narrow range. Drugs and neurogenic factors also influence renal hemodynamics. The renal circulation responds to changes in extracellular fluid volume, and in cardiac output. Renal ischemia occurs readily as these parameters decrease and prompt correction of circulatory dynamics can restore renal blood flow and prevent tubular necrosis. With hypovolemia or heart failure, angiotensin II is a mediator of efferent arteriolar constriction promoting a proportionately greater fall in renal plasma flow than in glomerular filtration rate, thereby augmenting sodium reabsorption. With renal failure, glomerulotubular balance is affected conversely promoting sodium loss. Appreciating these distinctions allows recognition of inappropriate sodium retention or loss. With such data, prognosis can be estimated more accurately and attempts to restore circulatory dynamics can be guided.
Nephron 1981
PMID:Pathophysiology of renal hemodynamics. 726 10


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