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

The purpose of this investigation was to study the relationships between the contractile behavior of the heart and myocardial prostaglandins. Using an open-chest model in rabbits, we assayed the left ventricular tissue content to prostaglandins (PG) E and F2 alpha at various intervals following acute pressure overload created by graduated aortic stenosis. The results suggest that the rabbits could be divided into two distinct groups based on specific hemodynamic changes following coarctation (systolic and diastolic pressure, dP/dt, and contractility index). The first group included rabbits whose adaptation to pressure overload was expressed as a gradual increase in the contractility index. The second group was comprised of rabbits that developed heart failure following coarctation. The increase in contractility in response to overload in the first group was paralleled by an increase in the content of PGE and PGF 2 alpha in the left ventricle, whereas, in rabbits with heart failure, the prostaglandin level did not rise above that of the control hearts. It is suggested that an increased endogenous prostaglandin content may be an important factor in adaptation to acute overload.
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PMID:Heart adaptation to acute pressure overload: an involvement of endogenous prostaglandins. 44 4

Congestive heart failure (CHF) is characterized by activation of (i) vasopressor and antinatriuretic influences (ii) and by counter-activation of vasodilator natriuretic systems. The former comprise the sympathoadrenal, renin-angiotensin-aldosterone and arginine vasopressin systems, and possibly endothelin and withdrawal of endothelium dependent relaxing factor respectively. The latter include the prostaglandins (PGE-2, PGI-2), dopamine and atrial natriuretic factor. The response of the kidney to chronic heart failure, i.e. vasoconstriction and antinatriuresis, resembles the renal reaction to volume depletion. The adverse renal effects of ACE inhibitors in some patients with advanced congestive heart failure may be explained by lowering of renal perfusion pressure and dependence of glomerular filtration rate on angiotensin II.
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PMID:The kidney in congestive heart failure. 191 36

Hemodynamic and hormonal responses to captopril were measured in 10 patients with severe chronic heart failure poorly controlled by digitalis and diuretics. After administration of a 25-mg dose, stroke volume (SV) increased from 53 +/- 7 to 63 +/- 9 ml (p less than 0.05), while pulmonary wedge pressure (PWP) decreased from 20 +/- 2 to 14 +/- 2 mm Hg (p less than 0.01). The hemodynamic changes were associated with increases in plasma renin activity (PRA; p less than 0.05) and in plasma levels of a novel bicyclo-prostaglandin E2 metabolite (bicyclo-PGE-m; p less than 0.01), whereas norepinephrine (NE) showed a falling tendency. In general, basal hemodynamic and basal hormonal levels did not correlate. Captopril-induced changes in mean artery pressure (MAP) and mean pulmonary artery pressure (mPAP) were positively correlated to pre-captopril PRA (r = 0.74, p less than 0.01; r = 0.64, p less than 0.05) and to changes in PRA (r = 0.85, p less than 0.01; r = 0.80, p less than 0.01) with a similar trend for angiotensin II (AII); decreases of systemic vascular resistance were more pronounced in patients with higher control NE levels (r = 0.62, p less than 0.05), the reduction of NE levels being highest in patients with higher basal concentrations (p less than 0.001); the captopril-induced decreases of mPAP and PWP were inversely related to basal bicyclo-PGE-m levels (r = 0.60, p less than 0.05; r = 0.61, p less than 0.05), and changes in mPAP were closely related to basal ratios of AII/bicyclo-PGE-m (r = 0.67, p less than 0.01). Thus, captopril exerts its acute beneficial hemodynamic effect by inhibiting the generation of AII, associated with toning down of sympathetic stimulation and increased production of vasodilating prostaglandins, such as PGE2. The relation between AII and PGE2-counteracting substances-might determine the hemodynamic response to captopril in the patients.
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PMID:Endogenous prostaglandin E2 metabolite levels, renin-angiotensin system and catecholamines versus acute hemodynamic response to captopril in chronic congestive heart failure. 637 Apr 31

In a placebo-controlled, double-blind study, we investigated the hemodynamic effects of a single infusion of prostaglandin E ( 1 ) (PGE ( 1 ); 60 microg infused over a period of 2 hours, the unit dosage used in courses of treatment for peripheral occlusive arterial disease) in 20 patients with moderate to severe chronic heart failure (New York Heart Association functional class II or III). Ejection fraction before therapy was less than 55%, and average age was 58.4 +/- 10 years in these clinically stable patients. Nineteen patients had coronary heart disease and one patient had had myocarditis underlying heart failure. Hemodynamic data were obtained by right- and left-heart catheterization and by Doppler echocardiography. Blood pressure and pulse rate were measured manually. Intravenous infusion of 60 microg PGE ( 1 ) over a period of 2 hours did not significantly alter contractility or hemodynamics. Dp/dt max, dp/dt max/p and dp/dt DP40, measures of left ventricular contractility determined with a catheter-tip manometer, did not differ significantly over time in PGE ( 1 ) -treated patients and those who received placebo. Other measures also failed to reveal PGE ( 1 ) -induced myocardial effects. We conclude that it is safe to administer PGE ( 1 ) to patients with peripheral occlusive arterial disease irrespective of heart failure.
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PMID:Hemodynamic effects of a single intravenous infusion of prostaglandin E1 in patients with clinically moderate to severe chronic heart failure. 1042 34

Prostaglandin E ( 1 ) (PGE ( 1 ) ) is a naturally occurring paracrine hormone that is used pharmacologically for treatment of peripheral occlusive arterial disease and to maintain ductus-arteriosus patency in neonates with congenital heart disease until the primary condition is operable. PGE ( 1 ) treatment also has been associated with reduction in pulmonary arterial pressure and increase in cardiac output in patients with left ventricular failure. In contrast, in isolated cases, patients with heart failure reportedly have developed pulmonary edema while receiving PGE ( 1 ). Therefore, to better define the effect of PGE ( 1 ) in heart failure, this double-blind study investigated the effect of PGE ( 1 ) on extravascular lung water in intensive-care patients with severe heart failure (New York Heart Association [NYHA] classes III and IV) and slightly above-normal extravascular lung water. Intravenous infusion of 60 microg PGE ( 1 ) (Prostavasin; Schwarz Pharma, Monheim, Germany) over a period of 2 hours caused no significant change in lung water relative to the baseline values (9.8 +/- 4.3 mL/kg before the infusion, 9.3 +/- 3.2 mL/kg after 1 hour, and 9.4 +/- 3.5 mL/kg after 2 hours) or to values observed in placebo-treated patients (6.5 +/- 3.3 mL/kg before the infusion, 7.1 +/- 2.7 mL/kg after 1 hour, and 7.0 +/- 3.2 mL/kg after 2 hours). Thus, administration of PGE ( 1 ) is unlikely to cause or worsen pulmonary edema in patients with severe heart failure (NYHA classes III and IV).
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PMID:Effect of prostaglandin E1 on extravascular lung water in patients with severe heart failure. 1042 35

In the adult mammalian kidney, high levels of cyclooxygenase (COX)-2 expression can be detected in the macula densa and associated cortical thick ascending limb cells and medullary interstitial cells. In the renal cortex, COX-2 expression increases in high renin states, and selective COX-2 inhibitors significantly decrease plasma renin levels. In the medullary region of the kidney, the expression of COX-2 increases in response to a high-salt diet and water deprivation. The most important prostanoids in the kidney are prostaglandin (PG)I(2), or prostacyclin, and PGE(2). PGE(2) diminishes sodium reabsorption; thereby, its inhibition results in sodium retention that can manifest clinically in a variety of ways, such as peripheral edema, increased blood pressure (mainly in treated hypertensive patients), weight gain, and occasionally deterioration of heart failure. PGI(2) increases potassium secretion. As such, its inhibition can result in hyperkalemia, particularly in patients with underlying renal insufficiency. PGI(2) is also a potent vasodilator and helps maintain renal perfusion in conditions of decreased actual or effective circulating volume; its inhibition in such patients can result in acute renal failure. A variety of studies has been conducted to examine the effects of celecoxib and rofecoxib on renal function. These incorporate various study designs directly, making it virtually impossible to compare data across studies. It is apparent from such studies, coupled with published case reports, that the impact of both celecoxib and rofecoxib on renal function (including development of edema and hypertension) is similar to that of nonselective nonsteroidal anti-inflammatory drugs (NSAIDs). Studies comparing the 2 COX-2 inhibitors conflict in their interpretation. Overall, the data suggest similar effects on renal function among all NSAIDs when used at comparable doses.
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PMID:Cyclooxygenase-2 inhibition and renal physiology. 1190 56

Prostaglandin E(1) (PGE(1)) has been used to treat pulmonary hypertension and peripheral artery occlusive disease and has been successfully employed for pharmacological bridging to transplantation in patients with chronic end-stage heart failure. In addition to its vasoactive effects PGE(1) was shown to stimulate angiogenesis in animal models. Recently we showed that PGE(1)-induced angiogenesis in hearts of patients with ischemic heart disease. We proposed that the angiogenic action of PGE(1) is mediated by vascular endothelial growth factor (VEGF). In the present paper we studied a possible effect of PGE(1) on the expression of VEGF-1 in cultured human adult cardiac myocytes (HACM) and cultured human adult cardiac fibroblasts (HACFB), respectively, to identify a cellular source of VEGF-1 in patients treated with PGE(1). We also aimed to delineate mechanisms involved in a possible regulation of VEGF-1 by PGE(1) in these cells. When HACM, isolated from human myocardial tissue, were treated with PGE(1), a significant up to 3-fold increase in VEGF-1 production could be observed. These results could be confirmed on the level of specific mRNA expression as determined by real-time polymerase chain reaction. The effect of PGE(1) on VEGF-1 expression could be blocked by H089, an inhibitor of cAMP-dependent protein kinase A. In HACFB, also isolated from human myocardial tissue, no effect of PGE(1) on VEGF-1 production was seen. If this effect of PGE(1) is also operative in the in vivo situation, one could speculate that cardiac myocytes could be a cellular source of PGE(1)-induced VEGF-1 expression in patients treated with this drug.
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PMID:Prostaglandin E1 induces vascular endothelial growth factor-1 in human adult cardiac myocytes but not in human adult cardiac fibroblasts via a cAMP-dependent mechanism. 1508 13

Physiological fetal circulation requires patency of the ductus arteriosus. As gestation proceeds, the sensitivity of the ductus to dilating prostaglandins diminishes. The sensitivity to constricting agents like PGE-synthetase inhibitors, present in many analgetics, however, increases. Fetuses affected by an antenatal constriction of the ductus arteriosus (DC) may present with different signs of cardiac failure including dilated right ventricle, tricuspid regurgitation and abnormal venous Doppler. We report on four cases with prenatal DC, presenting at 34, 35, 36 and 37 weeks of gestation. They were referred to fetal echocardiography because of abnormal routine echo scans with unexplained signs of right heart decompensation. Three patients were medicated during pregnancy with either aspirin (low dose), metamizole or ibuprofen. One patient did not take any drugs, especially no pain medication drug in pregnancy. Immediate delivery was performed in all cases. The neonates were in a good condition; echocardiography showed different degrees of right heart hypertrophy which disappeared in all infants by the age of 3 months except in case 2. Unexplained fetal right heart decompensation requires detailed echocardiographic evaluation of the ductus arteriosus and a sophisticated medical history with regard to analgesics. In contrast to ibuprofen and high-dose aspirin, metamizole and low-dose aspirin have not yet been reported as possible agents constricting the fetal arterial duct. In any suspected context, early delivery as in our cases may save babies life. Any application of non-steroidal anti-inflammatory drugs in pregnancy requires close fetal follow-up due to their potentially life-threatening effect.
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PMID:Prenatal constriction of the fetal ductus arteriosus--related to maternal pain medication? 1585 32

Magnesium is a micronutrient essential for the normal functioning of the cardiovascular system, and Mg deficiency (MgD) is frequently associated in the clinical setting with chronic pathologies such as CHF, diabetes, hypertension, and other pathologies. Animal models of MgD have demonstrated a systemic pro-inflammatory/pro-oxidant state, involving multiple tissues/organs including neuronal, hematopoietic, cardiovascular, and gastrointestinal systems; during later stages of MgD, a cardiomyopathy develops which may result from a cascade of inflammatory events. In rodent models of dietary MgD, a significant rise in circulating levels of proinflammatory neuropeptides such as substance P (SP) and calcitonin gene-related peptide among others, was observed within days (1-7) of initiating the Mg-restricted diet, and implicated a neurogenic trigger for the subsequent inflammatory events; this early "neurogenic inflammation" phase may be mediated in part, by the Mg-gated N: -methyl-D-aspartate (NMDA) receptor/channel complex. Deregulation of the NMDA receptor may trigger the abrupt release of neuronal SP from the sensory-motor C-fibers to promote the subsequent pro-inflammatory changes: elevations in circulating inflammatory cells, inflammatory cytokines, histamine, and PGE(2) levels, as well as formation of nitric oxide, reactive oxygen species, lipid peroxidation products, and depletion of key endogenous antioxidants. Concurrent elevations of tissue CD14, a high affinity receptor for lipopolyssacharide, suggest that intestinal permeability may be compromised leading to endotoxemia. If exposure to these early (1-3 weeks MgD) inflammatory/pro-oxidant events becomes prolonged, this might lead to impaired cardiac function, and when co-existing with other pathologies, may enhance the risk of developing chronic heart failure.
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PMID:The nerve-heart connection in the pro-oxidant response to Mg-deficiency. 1681 76

There has been increasing evidence that tumor necrosis factor alpha (TNF-alpha) is synthesized by cardiomyoctes and contributes to their impaired function and to cardiac failure. Because the Na(+)-K(+) ATPase is a key player in the contraction of cardiomyocytes, this work was undertaken to study the effect of TNF-alpha on the Na(+)-K(+) ATPase in rat heart. Sprague Dawley rats (Rattus norvegicus) were injected with TNF-alpha (270 ng/100 g body weight) and 4 h later the ventricles were isolated, homogenized and assayed for their Na(+)-K(+) ATPase activity. The effect of TNF-alpha on the pump was studied also in isolated myocytes treated in suspension. The involvement of PGE2 was investigated by pre-treating animals or cells with indomethacin, an inhibitor of COX enzymes. The involvement of NF-kappaB and AP-1 was studied using their respective inhibitors PDTC and curcumin. A time response study showed an increase in the activity of the Na(+)-K(+) ATPase in the left and right ventricles of animals treated with the cytokine, with no change in its protein expression. This effect disappeared in the presence of indomethacin suggesting an involvement of PGE(2) in the action of TNF-alpha. Rats and cells treated directly with PGE(2) showed a dose-dependent response. A decrease in the activity of the Na(+)-K(+) ATPase was observed at a low dose and an increase at a high dose in both ventricles. Since PGE(2) is suspected to be the active mediator in TNF-alpha signaling, inhibiting its synthesis by inhibiting some suspected transcription factors was attempted. PDTC abrogated fully, and curcumin partially the effect of the cytokine. It was concluded that TNF-alpha activates NF-kappaB and AP-1 and induces PGE(2) release which alters dose-dependently the activity of the pump by activating different EP receptors with different affinities for PGE(2).
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PMID:Tumor necrosis factor alpha alters Na+-K+ ATPase activity in rat cardiac myocytes: involvement of NF-kappaB, AP-1 and PGE2. 1702 35


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