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

Ultrafiltration improves the clinical condition of patients with congestive heart failure (CHF) through a reduction of excessive body water. We investigated the relationships among intra and extravascular fluids, hemodynamics and neurohumoral pattern following plasma water subtraction. In 55 patients with CHF (35 in NYHA class IV, Group A, and 20 in NYHA class II-III, Group B), removal of 3242 +/- 201 ml and 1741 +/- 119 ml of plasma water acutely reduced plasma volume (calculated from hematocrit changes) by -20.7% and -12.9% in Group A and in Group B, respectively. Plasma volume returned to baseline values within 48 hours. Body weight and ventricular filling pressures also lowered and remained so for 2 days. After ultrafiltration urinary output increased and norepinephrine, renin activity and aldosterone plasma levels decreased in Group A, while a fall of diuresis and a rapid rise of plasma levels of the 3 hormones were observed in Group B. Two days after ultrafiltration the persistence of reduced body weight with recovery of plasma volume indicates a shift of fluid from the extravascular to the intravascular compartment. The different behaviour of hemodynamics, urinary output and neurohumoral pattern changes observed in the 2 groups after ultrafiltration, suggest that in severe heart failure (Group A) the physiological responses to intravascular volume depletion are unsettled while are preserved in less severe stages of the disease (Group B).
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PMID:[Interrelation of plasma volume, fluid metabolism and neurohormonal activation after ultrafiltration in congestive heart failure]. 136 83

The cardiovascular effects of NKH477 (6-(3-dimethylaminopropionyl)forskolin hydrochloride), a novel water-soluble forskolin derivative, were investigated in dogs. Intravenous (i.v.) injections of NKH477 (1-30 micrograms/kg) caused dose-related increases in left ventricular dP/dtmax (LVdP/dtmax), coronary and femoral artery blood flow (CBF, FBF), heart rate (HR), and myocardial oxygen consumption (MVO2) and a dose-related decrease in blood pressure (BP) in anesthetized dogs. The regression analysis between CBF and MVO2 showed that NKH477 did not influence substantially the balance of oxygen supply and demand. Infusions of NKH477 (0.15-0.6 microgram/kg/min i.v.) also increased LVdP/dtmax, cardiac output (CO), and HR and decreased BP, pulmonary arterial diastolic pressure, and total peripheral resistance (TPR) in a dose-dependent manner. In contrast to forskolin, NKH477 administered intraduodenally (0.05-0.2 mg/kg) and orally (0.15 and 0.3 mg/kg) clearly exhibited cardiovascular actions, as it did in i.v. administration, indicating that NKH477 is orally active. No arrhythmias were induced by NKH477 in any study. NKH477, like forskolin, showed adenylate cyclase stimulant activity in guinea pig ventricular membrane but did not inhibit Na+, K(+)-ATPase or phosphodiesterase (PDE) activity. Thus, NKH477 can be characterized as a potent, orally active, water-soluble forskolin derivative, which suggests that NKH477 is a useful inodilator for treatment of heart failure, especially in the severe stage with beta-adrenoceptor downregulation.
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PMID:Cardiovascular and adenylate cyclase stimulant properties of NKH477, a novel water-soluble forskolin derivative. 138 Jun 7

In this study the effect of the angiotensin converting enzyme (ACE) inhibitor captopril on beta-receptor responsiveness was investigated in failing rat hearts after experimental myocardial infarction. Infarcted rats were treated for 8 weeks with either captopril added to the drinking water (100 mg/kg/day; n = 5) or drinking water alone (n = 7). Treatment was started 2-3 days before myocardial infarction. A third group of untreated rats without myocardial infarction served as control (n = 6). At the end of the treatment period the hearts were perfused as described by Langendorff, and a cumulative dose-response curve of isoprenaline was obtained in each heart. In comparison with noninfarcted hearts, the response of heart rate and peak pressure rate (dP/dt) to isoprenaline stimulation was significantly depressed in hearts of infarcted rats. Chronic treatment with captopril significantly attenuated the reduced responsiveness to isoprenaline stimulation. This improved responsiveness in captopril-treated rat hearts might be due to prevention of "down-regulation" of myocardial beta-adrenoceptors. Other factors should also be considered, such as prevention of structural alterations in the noninfarcted myocardium, e.g., myocardial hypertrophy and fibrosis. Differences in infarct size did not play an important role, since infarct size was comparable in both groups of infarcted rats. This partial preservation of beta-adrenergic responsiveness was accompanied by a significant reduction in right ventricular weight and lung weight, suggesting that captopril also improved the signs of heart failure. Therefore, the results of this study indicate that early ACE inhibition in myocardial infarction may be useful in preventing deterioration of cardiac function.
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PMID:Captopril modifies the response of infarcted rat hearts to isoprenaline stimulation. 138 72

The intrarenal renin-angiotensin system (RAS) may contribute to the pathophysiology of heart failure by the generation of angiotensin II at local sites within the kidneys. Angiotensin II may directly influence renal hemodynamics, glomerular contractility, and tubular sodium reabsorption, thereby promoting sodium and fluid retention in this syndrome. In the present study, we examined components of the circulating RAS as well as the intrarenal expressions of renin and angiotensinogen mRNA in rats with stable compensated heart failure (HF) 12 wk after experimental myocardial infarction. Renal angiotensinogen mRNA level in vehicle-treated HF rats increased 47%, as compared with sham control rats (P = 0.001). The increase in angiotensinogen mRNA levels was more pronounced in animals with medium (46%, P < 0.05) and large (66%, P < 0.05) infarcts than in those with small infarcts (31%, P = NS). There were no differences in liver angiotensinogen mRNA, circulating angiotensinogen, angiotensin II, plasma renin concentration (PRC), kidney renin content (KRC), and renal renin mRNA level between sham and HFv. In addition, in a separate group of rats with heart failure, we demonstrated that renal angiotensin II concentration increased twofold (P < 0.05) as compared with that of age-matched sham operated controls. A parallel group of heart failure rats (HFe, n = 11) was treated with enalapril (25 mg/kg per d) in drinking water for 6 wk before these measurements. Blood pressure decreased significantly during treatment (91 vs. 103 mm Hg, P < 0.05). Enalapril treatment in HF rats increased renin mRNA level (2.5-fold, P < 0.005), KRC (5.6-fold, P = 0.005), and PRC (15.5-fold, P < 0.005). The increase in renal angiotensinogen mRNA level observed in HFv rats was markedly attenuated in enalapril treated HF rats (P < 0.001), suggesting a positive feedback of angiotensin II on renal angiotensinogen synthesis. These findings demonstrate an activation of intrarenal RAS, but no changes in the circulating counterpart in this model of experimental heart failure, and they support the concept that the intrinsic renal RAS may contribute to the pathophysiology in this syndrome.
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PMID:Evidence for tissue-specific activation of renal angiotensinogen mRNA expression in chronic stable experimental heart failure. 140 Oct 84

Studies over the past 10 years suggest that the atrial natriuretic factor (ANF) plays an important role in salt and water homeostasis. Responding to atrial stretch, the atria releases ANF into the circulation. The several actions of this hormone tend to increase renal NaCl excretion resulting in reduced blood volume and blood pressure. ANF increases the glomerular filtration rate and reduces sodium chloride reabsorption in the distal nephron. It also inhibits secretion of aldosterone from the adrenal cortex. Therefore actions of ANF appear to be opposed to the renin-angiotensin-aldosterone system. Drugs that alter ANF metabolism may constitute a new mechanism of treatment for hypertension and heart failure.
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PMID:Role of atrial natriuretic factor in salt and water homeostasis. 140 80

The efficacy of NKH477, a novel water-soluble forskolin derivative, in improving cardiac failure was assessed in dog heart-lung preparations. Cardiac functions depressed by pentobarbital, propranolol or verapamil so that cardiac output had been reduced by about 40-50% of the respective control were all improved by NKH477 (10-100 micrograms) in a dose-dependent manner. With 100 micrograms NKH477, almost complete restoration of cardiac performance was attained in the respective cardiac failures. In the combination of NKH477 with ouabain (30 micrograms), 30 micrograms of NKH477 completely restored the cardiac function depressed by pentobarbital, associated with a slight but not significant increase in heart rate. No arrhythmias were induced by any of the NKH477 doses used in the experiments. These results suggest that NKH477 should be subjected to clinical trials in the treatment of cardiac failure.
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PMID:Improvement of drug-induced cardiac failure by NKH477, a novel forskolin derivative, in the dog heart-lung preparation. 140 34

Understanding of heart failure has developed through 3 paradigms involving organ, cell, and gene. The first views heart failure as an abnormality of organ (pump) function leading to salt and water retention and vasoconstriction. Therapy to correct these circulatory abnormalities is well accepted and effective. The second considers heart failure as a disordered cellular function, mainly impaired contraction and relaxation. Efforts to correct the biochemical and biophysical abnormalities responsible for these disorders of myocardial performance have, however, been less successful. Recent emphasis on efforts to improve prognosis as well as symptoms in patients with chronic heart failure demonstrates that it is a lethal disease with problems of survival similar to those in malignancies. The third paradigm of abnormal gene expression, which in the failing heart represents a cardiomyopathy of overload, appears to be a major cause of poor prognosis in these patients. Evidence that the angiotensin-converting enzyme inhibitors have important effects on cell growth, as well as on vascular tone, suggests that their ability to prolong survival in patients with heart failure may be due largely to the inhibition of detrimental effects of angiotensin II on cardiac gene expression. Thus, it seems likely that work focused on the third paradigm will uncover specific abnormalities of gene expression that are responsible for poor survival of patients with heart failure. By 2001, I predict that heart failure will be viewed as an abnormality of cell growth and this will lead to the development of therapies to retard, if not reverse, the clinical deterioration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heart failure in 2001: a prophecy. 1139 58

We investigated the role of atrial natriuretic factor (ANF) and the renin-angiotensin system as well as the effects of losartan in rats with aortocaval (AC) shunts. Right atrial and left ventricular end-diastolic pressures (LVEDP) were higher and mean arterial blood pressure (MAP) was lower in AC shunt animals than in their controls. AC shunt rats presented marked cardiac hypertrophy, decreased right atrial ANF concentration, and increased ventricular ANF content and concentration. Plasma ANF levels were elevated, and hematocrit was lower in AC shunt animals than in controls. Captopril or losartan treatment decreased MAP and returned LVEDP to sham-operated control values. A clear regression of cardiac hypertrophy was evident in both treated AC shunt groups, with plasma ANF levels tending to follow those in sham-operated rats. Plasma COOH-terminal ANF levels were decreased and urinary volume and hematocrit were increased in losartan-treated AC shunt animals. We conclude that chronic angiotensin converting enzyme inhibition and angiotension II receptor antagonism improved hemodynamic conditions, diminished water retention, reversed cardiac hypertrophy, and restored plasma and tissue ANF to more "normal" levels in rats with moderate high-output heart failure.
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PMID:Chronic captopril and losartan (DuP 753) administration in rats with high-output heart failure. 141 10

Acute renal insufficiency after cardiopulmonary bypass can lead to a significant morbidity from fluid overload and electrolyte disturbance, impede pulmonary gas exchange, and postpone weaning from mechanical ventilation. The limitations placed on free water intake result in severe restriction of nutrition while diuretic therapy causes electrolyte imbalance. Artificial renal support either in the form of peritoneal dialysis or hemodialysis may be complicated by sepsis and hemodynamic instability. We reviewed our experience with the use of continuous arteriovenous hemofiltration, an extracorporeal technique for removal of solutes, toxins, and water in critically ill patients with cardiac failure complicated by acute renal insufficiency and hemodynamic instability after cardiopulmonary bypass. Ten infants and children with renal insufficiency caused by low cardiac output had continuous arteriovenous hemofiltration instituted for indications including sepsis, volume overload, oliguria for more than 24 hours nonresponsive to diuretic therapy, and the need for hyperalimentation. All were supported by mechanical ventilation and receiving high-dose inotropic support. Arterial and venous vascular access was successfully obtained by cannulation of the femoral artery and vein in nine patients. Anticoagulation of the circuit was achieved with heparin infusion (6 to 20 micrograms/kg/hr) and monitored by measurement of activated clotting time. The continuous arteriovenous hemofiltration circuit was replaced if there was clot formation, or at 3 days after placement. Dialysis solution (Dianeal) 1.5% or 0.5% was infused as prefilter dilution. With the use of continuous arteriovenous hemofiltration, 20 to 100 m/hr of ultrafiltrate was removed, which allowed correction of hypervolemia, and caloric intake increased from 13.5 kcal/kg/day to 79.5 kcal/kg/day. Continuous arteriovenous hemofiltration was maintained between 5 hours and 8 days and was well tolerated in all patients. Serum urea and creatinine levels declined during continuous arteriovenous hemofiltration. We conclude that continuous arteriovenous hemofiltration is a safe and effective method for fluid and electrolyte homeostasis and that it thus allows hyperalimentation in infants and children after cardiac operations.
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PMID:Continuous arteriovenous hemofiltration after cardiac operations in infants and children. 143 99

In this study, we tested the hypothesis that erythrocyte deformability is decreased in the development of cardiac failure induced by NaCl toxicosis. Deformability of erythrocytes and routine hematologic and biochemical variables were measured in 6 of 50 chickens that were given 5 g of NaCl/L in their drinking water from day 7 to day 42, and were compared with values in 6 of 50 healthy chickens given free access to tap water. Deformability was assessed by passing a 10% suspension of erythrocytes through a polycarbonate membrane with 5-microns pores. Chickens were euthanatized and heart and body weights were determined. Treatment with NaCl induced right-sided cardiac failure up to day 28. The ratios of heart weight to body weight were greater, for right ventricle by 20 to 64% and for left ventricle by 15 to 27%, attributable to NaCl treatment. Deformability of erythrocytes of NaCl-treated chickens was markedly decreased, in association with increased erythrocyte size and plasma Na+ concentration. However, only part of the decreased deformability could be explained by swelling of erythrocytes. Decreased deformability could not be explained by increased cell viscosity because mean corpuscular hemoglobin concentration, the primary determinant of erythrocyte viscosity, was decreased. Because decreased deformability of erythrocytes has been demonstrated previously to be associated with increased vascular resistance, decreased deformability may have contributed to the development of right-sided cardiac failure in these chickens.
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PMID:Changes in erythrocyte deformability in NaCl-induced right-sided cardiac failure in broiler chickens. 147 22


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