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

This study examines whether the alpha 1-adrenoceptors in canine endothelium-denuded dorsal pedal artery and endothelium-denuded saphenous vein can be differentiated by 5-methyl-urapidil before (non-paced) and at end-stage heart failure induced by rapid ventricular pacing. Noradrenaline and phenylephrine produced concentration-dependent contractions of the dorsal pedal artery and the saphenous vein which were enhanced at end-stage heart failure. In non-paced animals, 5-methyl-urapidil was shown to be insurmountable against noradrenaline with the artery being more sensitive compared to the vein. At end-stage heart failure, 5-methyl-urapidil was a competitive antagonist against noradrenaline in both the artery and the vein with pA2 values of 8.1 (7.9-8.4) and 8.6 (8.2-9.1), respectively. A different antagonist profile was seen against phenylephrine. Similar to noradrenaline, insurmountable antagonism was observed in the artery and the vein before the development of heart failure. In contrast to noradrenaline, at end-stage heart failure, no antagonism was seen with the concentrations of 5-methyl-urapidil tested against phenylephrine. These results suggest that the mechanisms mediating contractions in the dorsal pedal artery and saphenous vein to noradrenaline and phenylephrine are heterogeneous and dependent on the heart failure state.
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PMID:Interaction of 5-methyl-urapidil with alpha 1-adrenoceptors in canine blood vessels: impact of pacing-induced heart failure. 900 13

Norepinephrine and epinephrine stimulate alpha- and beta-adrenergic receptors which, in turn, modulate force of contraction in heart muscle cells. However, chronic stimulation may be associated with growth-promoting effects and modulation of the cardiac phenotype. Sympathetic tone is chronically enhanced in chronic heart failure and results in a selective down regulation of beta 1 adrenergic receptors, most likely due to local mechanisms. Beyond reduced beta 1 receptor density and increased levels of inhibitory Gi proteins, there is now evidence that NO can modulate the beta-adrenergic stimulation in the human myocardium. Increased NO activity generated by an inducible NO synthase is associated with a reduced positive inotropic response to beta-agonists, a mechanism which may play an important role in inflammatory states such as myocarditis or sepsis. Experimental data suggests that stimulation of alpha-adrenergic receptors of cardiomyocytes results in cardiac growth and changes in phenotype which, in turn, may affect the functional properties of the myocardium. For example, phenylephrine can upregulate the expression of the sodium/calcium exchanger, while the expression SR Ca2+ ATPase may be reduced. The latter is also affected by angiotensin II. Similar changes in the expression of these crucial proteins for the cardiac calcium homeostasis have been reported in the failing human heart, raising the possibility that the increased sympathetic tone and the activated renin-angiotensin system may be involved in these changes.
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PMID:[Sympathetic nervous system in heart failure: effect of catecholamines and nitric oxide]. 906 72

Glomerular volume has been reported to be increased in patients with congenital cyanotic heart disease and cor pulmonale; however it has not been systematically studied in patients with congestive cardiac failure (CCF). Glomerular volume was therefore measured by point-counting serially sectioned glomerular profiles of 25 randomly selected glomeruli using the Cavalieri principle in autopsy specimens from 8 patients dying from CCF and 6 age-matched controls with no renal or cardiac pathology. Mean glomerular volume was not different between patients dying from CCF and controls, 2.49 (0.21) vs. 2.25 (0.26) x 10(6) microm3, and the distribution of individual glomerular volumes was similar in the two groups. We conclude that severe CCF is not associated with significant glomerular enlargement and that the previously reported glomerular enlargement in cyanotic heart disease is likely to be mediated through hypoxemia.
Nephron 1997
PMID:Glomerular volume in congestive cardiac failure. 920 Apr 4

Norepinephrine (NE) (2.5 micrograms/kg/min) was administered to 5-week-old male Sprague Dawley rats by subcutaneous osmotic mini pumps for 14 days to generate an in vivo cardiac hypertrophy model and the responses with respect to aging examined. In the model, ventricles were significantly hypertrophied without myocardial necrosis and without significant increases in heart rate or blood pressure; the beta adrenergic system was down-regulated. In 37-week-old rats receiving 1.0 microgram/kg/min NE, there was a tendency towards heart failure, and myocardial necrosis and interstitial fibrosis were revealed by histological examinations. The density of beta adrenergic receptors and adenylyl cyclase activity was lower in the older rats. The excess stimulation of adrenergic receptors caused severe cardiac injury in old rats regardless of down regulation of beta adrenergic receptors.
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PMID:Age-related effects of norepinephrine on rat ventricular hypertrophy. 929 May 77

We have examined the ryanodine receptor, Ca(2+)-ATPase, calsequestrin and phospholamban mRNA levels in the left ventricles of pacing-induced heart failure and norepinephrine infusion dogs. The heart failure dogs showed a decrease in the levels of ryanodine receptor and Ca(2+)-ATPase mRNAs. Norepinephrine infusion caused a reduction of Ca(2+)-ATPase mRNA but no change in ryanodine receptor mRNA. There was a corresponding reduction of the immunoreactive Ca(2+)-ATPase protein levels in both heart failure and norepinephrine infusion animals compared to controls. In contrast, the mRNAs of calsequestrin and phospholamban were unchanged in dogs with either congestive heart failure or norepinephrine infusion. Thus, since norepinephrine infusion and congestive heart failure produced similar reductions of Ca(2+)-ATPase mRNA and protein, we postulate that the down-regulation of Ca(2+)-ATPase in congestive heart failure may be caused, at least in part, by sympathetic stimulation that occurs in heart failure.
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PMID:Altered sarcoplasmic reticulum Ca2+ ATPase gene expression in congestive heart failure: effect of chronic norepinephrine infusion. 950 Aug 74

The QTc dispersion reflects the underlying regional heterogeneity of the recovery of the ventricular excitability, thereby it is considered as a novel marker of risk of ventricular arrhythmias. Because a higher incidence of ventricular arrhythmias is described during and after hemodialysis, the aim of this study has been to evaluate the QTc dispersion before and after uncomplicated hemodialysis session. Twenty chronic uremics without heart failure, ischemic heart disease or dialysis hypotension were selected. The QTc dispersion was determined as the difference between the longer and the shorter QTc interval measured on a 12-lead electrocardiogram. Following the hemodialysis session, the QTc dispersion increased from 30 +/- 9 to 54 +/- 17 ms (p < 0.001) associated with the expected reduction of potassium and magnesium and with the increase of extracellular calcium concentration. However, no correlation has been observed between the QTc dispersion increase and the degree of the intradialytic changes of plasma electrolytes, blood pressure or body weight. In summary, the hemodialysis treatment per se does induce an increase of the QTc dispersion, likely due to the rapid changes of electrolyte plasma concentrations. This can potentially contribute to the arrhythmogenic effect of the hemodialysis procedure, reflecting an enhanced regional heterogeneity of ventricular repolarization. The clinical importance of the increase of QTc dispersion as risk factor of ventricular arrhythmias, particularly in hemodialyzed patients suffering from ischemic or hypertrophic heart diseases, should be the matter of further investigations.
Nephron 1998
PMID:Effect of hemodialysis on the dispersion of the QTc interval. 1039 2

Fish venoms can be lethal for Vertebrates. The effect depends of dose and subject, more than incriminated fish. The most constant symptom is a violent pain; but the serious pharmacological effects are respiratory and heart failure with marked hypotension and cardiac perturbations, neurologic damage, such as seizure and coma. Experimentation is difficult due to venom instability. Activity is lost by distilled water, lyophilisation in buffers, several successive freezing and defreezing. In addition, when venom is broken, other pharmacological effects are evidenced, for instance, with Synanceia verrucosa venom, hypertensive phase takes the place of hypotension. It is difficult to distinguish toxin effect from this of denaturation products of the toxin. Noradrenaline is present in Synanceia venom, and it seems that acetylcholine exists in some venom, at least when diluted in saline solution. Other biological active products are present. Purified toxins allow pharmacological investigations. Stonefish venom is better studied, because venomous glands contain relatively high venom quantity. Stonustoxin from Synanceia horrida exerts its action through NO-synthase liberation, and its primary action can be attributed to its potent vasorelaxant activity, causing a rapid, marked and irreversible hypotension. Trachynilysin, from Synanceia trachynis, causes massive release and depletion of acetylcholine and damage to nerve and muscle fibres, which can account for the inhibition of neuromuscular function, and skeletal paralysis. But the used doses are not compatible with respiratory arrest. Verrucotoxin from Synanceia verrucosa activates potassium channels dependent from ATP; this can explain damage, and probably neurologic and respiratory distress.
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PMID:[Pharmacological properties of fish venoms]. 975 86

Treatment of patients with severe heart failure by ACE inhibition is often limited by worsening of renal function. To evaluate whether trandolapril, a potent lipophilic ACE inhibitor, affects renal function in severe heart failure, we studied 12 patients with severe heart failure treated with only diuretics and digoxin. Patients received increasing oral dosages of trandolapril (0, 1, and 2 mg) on 3 consecutive days (A). Patients were then discharged on 2 mg trandolapril bid and re-evaluated 8 weeks later (B). Mean arterial and pulmonary wedge pressures decreased by maximal 14% and 43%, and stroke volume and work indexes increased by 24% and 20% at A and similarly at B (11, 45, and 25 ns and 33%, respectively). In contrast, heart rate, systemic resistance, pulmonary artery pressure, and cardiac index decreased by 6%, 23%, 29%, and 17%, respectively, at only A. Renal blood flow improved by approximately 40% both at A and B. In contrast, the glomerular filtration rate decreased by 25% at only B, whereas serum creatinine, creatinine clearance, and urine osmolality were unaffected during the study. Norepinephrine, angiotensin II, and aldosterone levels decreased by approximately 30%, 60%, and 65%, respectively, at both A and B. Renin levels increased by 136% at A and remained elevated at B. Thus, whereas the initial systemic vasodilating and inotropic effects did not persist, long-term trandolapril results in sustained neurohormonal modulation, reduced preload, and improved organ perfusion, indicated by a persistent increase in renal blood flow and preservation of renal function in severe heart failure.
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PMID:Renal hemodynamic effects in patients with moderate to severe heart failure during chronic treatment with trandolapril. 982 86

Since 1992, adrenalectomy for pheochromocytoma has been recognized as a safe and efficient technique when performed by a laparoscopic approach. Most of the cases of pheochromocytomas treated as such and published in the literature were not associated with malignant hypertension and acute heart failure. We report the case of a 23-year-old woman who presented with this clinical picture and show that laparoscopic adrenalectomy may be as safe and efficient as conventional adrenalectomy when performed in this situation. The intraoperative changes in the secretion of catecholamines, endothelin-1, angiotensin II, N- and C-terminus of atrial natriuretic factor prohormone were also analyzed. Noradrenaline release during tumor dissection was associated with a stimulation of atrial natriuretic factor.
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PMID:Heart failure induced by pheochromocytoma: laparoscopic treatment and intraoperative changes of several new cardiovascular hormones. 1009 71

Excessive neurohumoral activity remains a major burden to the circulation of patients with advanced heart failure. Prostaglandin E1 (PGE1), a balanced i.v. vasodilator, was shown to elicit favorable hemodynamic and clinical effects in this cohort. A prospective randomized parallel group trial was performed to evaluate acute, intermediate and chronic changes in hemodynamic, neurohumoral and renal variables in response to PGE1, dobutamine and placebo. Thirty patients with class III and IV heart failure and low cardiac index (mean 1.9 l/min/m2) two hours after oral drugs including high dose enalapril were included. A 7-day-infusion of PGE1 (16.5 +/- 5 ng/kg/min, range 10 to 20 ng/kg/min, group A n = 10), dobutamine (4.5 +/- 1 micrograms/kg/min, range 2.5 to 5 micrograms/kg/min, group B n = 10) or placebo (saline, group C n = 10) was administered via a central venous access line after stepwise titration until intolerable side effects developed with PGE1 or a 20% increase in cardiac index occurred with dobutamine, which was continued on this dose throughout while PGE1 was maintained on 50% peak dose. Hemodynamic data were collected at baseline, at peak dosages, after 12 hours and after 7 days. Of neurohumoral variables plasma norepinephrine, big endothelin (Big ET) and atrial natriuretic peptide (ANP) were simultaneously evaluated using RIA methods. Renal plasma flow (by paraaminohippurate clearance) and glomerular filtration rate (by iothalamate clearance) was measured prior to and during the infusions (after 12 hours and after 7 days). At peak dose and at 12 hours significant drops from baseline of mean pulmonary artery pressure, pulmonary capillary wedge pressure and systemic vascular resistance were observed which were accompanied by a rise in cardiac output with both PGE1 and dobutamine. These changes were maintained through 7 days when pulmonary vascular resistance levels also fell with both active drugs. Blood pressure did not change throughout, but PGE1 increased heart rate slightly at 12 hrs. Both PGE1 and dobutamine enhanced renal plasma flow after 7 days, but only PGE1 decreased glomerular filtration fraction significantly. Glomerular filtration rate did not change with either drug. PGE1 decreased ANP levels at 12 hrs, and dobutamine increased big ET levels at peak, but decreased big ET at 7 days. Norepinephrine levels were unaffected throughout. Except a slight decrease in right atrial pressure after 7 days placebo did not change any measured variable significantly. Taken together, these data suggest that treatment with PGE1 is as efficacious as low-dose dobutamine in improving cardiac performance and renal perfusion in advanced heart failure. Of importance, no deleterious neurohumoral counterregulation was observed with PGE1.
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PMID:Effects of prostaglandin E1, dobutamine and placebo on hemodynamic, renal and neurohumoral variables in patients with advanced heart failure. 1050 54


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