Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Following surgery for congenital heart disease, there is often an increased reactivity of the pulmonary vasculature to stimuli, resulting in rapid increases in pulmonary artery pressure and a clinical impression of stiff lungs. Lung mechanics were measured in 30 children, mean age 6.7 +/- 4.1 mo, who were ventilated and had pulmonary artery pressure monitoring following surgery for congenital heart disease. A group of 15 patients developed postoperative pulmonary hypertension. In these patients, respiratory system resistance was 43% higher (p = 0.001) and compliance 11% lower (p = 0.004) during acute pulmonary hypertension compared with baseline pulmonary artery pressure. No changes in resistance or compliance were seen in the 15 patients who did not develop pulmonary hypertension. The changes in lung mechanics interfered with mechanical ventilation, resulting in a 9.4% rise in PaCO2 during pulmonary hypertension. The bronchial smooth muscle was found to be increased by 68%, and the vascular smooth muscle was more than twice normal in lung biopsies from 9 pulmonary hypertension patients compared with 6 age-matched postmortem controls patients who had no cardiac or pulmonary disease. The bombesin-immunoreactive pulmonary neuroendocrine cells (PNEC) were also increased in the pulmonary hypertension patients. These findings suggest a coconstriction and cohypertrophy of bronchial and vascular smooth muscle during pulmonary hypertension. Mediators, such as bombesin, endothelin-1, and serotonin, are known to be produced by PNEC and may be involved in the observed vasoconstriction, increased respiratory system resistance, and smooth muscle hypertrophy.
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PMID:Increased respiratory system resistance and bronchial smooth muscle hypertrophy in children with acute postoperative pulmonary hypertension. 755 93

Endothelin is a powerful vasoconstrictor that may be partly responsible for the increases in venous and arterial tone characteristic of heart failure. The release of endothelin from endothelial cells in culture is stimulated by angiotensin II. We investigated the relationship between plasma concentrations of immuno reactive endothelin-1 and angiotensin II in 25 patients with heart failure and eight with ischaemic heart disease but normal left ventricular function. Plasma concentrations of endothelin and angiotensin II were correlated (Spearman rank correlation coefficient of 0.72; P < 0.0001) in patients with heart disease. Plasma concentrations of angiotensin II and endothelin were higher in those patients with heart failure. Angiotensin II was infused over a 3 h period in eight healthy volunteers. Infusion of angiotensin II increased plasma concentrations of angiotensin II to levels greater than those usually found in patients with severe heart failure but induced only a modest rise in plasma concentrations of immunoreactive endothelin-1 (0.77 +/- 0.16 to 1.03 +/- 0.03 pmol.l-1, P < 0.02). Increased plasma concentrations of angiotensin II and endothelin-1 both appear to reflect the presence and severity of heart failure. Although a significant correlation exists between plasma concentrations of angiotensin II and endothelin in patients with heart failure, the relationship may not be causal.
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PMID:Elevated plasma endothelin concentrations in heart failure; an effect of angiotensin II? 769 33

Neurally mediated syncope is the most frequent cause of syncope in patients who do not have structural heart disease. Neurally mediated syncope is believed to be a reflex triggered by excessive afferent discharge from mechanoreceptors located in the arterial tree or viscera, particularly the left ventricle of the heart. In response to these signals, a CNS-mediated sudden rise in parasympathetic efferent activity occurs, causing relative or absolute bradycardia and sympathoinhibition with arterial vasodilation and hypotension. Although our understanding of the pathophysiology of this syndrome is still incomplete, it is well established that sympathetic nerve activity and norepinephrine release fall inappropriately during neurally mediated syncope, whereas appropriate increases in plasma concentrations of epinephrine, angiotensin II, vasopressin, and endothelin-1 occur. Recent studies from our laboratory suggest that synthesis of the vasodilator nitric oxide increases during neurally mediated syncope. This suggests that nitric oxide-mediated arterial vasodilation could contribute to the profound hypotension characteristic of this syndrome. The diagnosis of neurally mediated syncope can be made with acceptable levels of specificity and sensitivity by the upright tilt test. Explaining the mechanisms responsible for arterial vasodilation in neurally mediated syncope may lead to effective treatment.
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PMID:Neurally mediated syncope: pathogenesis, diagnosis, and treatment. 774 68

In 77 children with congenital heart disease urinary endothelin-1 (ET-1), an indicator of intrarenal endothelin release, was compared to urinary excretion of total protein, albumin, immunoglobuline G (IgG), alpha 1-microglobuline (alpha 1-MG), N-acetyl-beta-D-glucosaminidase (NAG) and villin. Urine samples were collected the day before and immediately after cardiac angiography with high (Conray 70; n = 56; CON) or low osmolality contrast media (Solutrast 300; n = 21; SOL) to assess the relationship between urinary endothelin and glomerular and tubular nephrotoxicity of contrast media. The children were further subdivided according to age: less than 1 year-CON 1 (n = 20); SOL 1 (n = 12) and 1-18 years CON 2 (n = 36); SOL 2 (n = 9). Results (median): 1. There are no significant changes in total protein-, albumin- and IgG-excretion as parameters of glomerular toxicity. 2. Tubular toxicity of contrast media is shown by significant increase of alpha 1-MG-(10.0 to 23.2 mg/g Crea; p < 0.001), NAG-(5.9 to 9.6 mg/g Crea; p < 0.001) and Villin-excretion (1.0 to 2.0 STS, p < 0.001) in all children. 3. Endothelin excretion (101.0 to 163.0 ng/g Crea, p < 0.001) and concentration (42.5 to 56.0 pg/ml; p < 0.001) were elevated after angiography in all children. 4. The changes in endothelin excretion are correlated to the changes in alpha 1-MG (r = 0.65; p < 0.001) and NAG (r = 0.43, p < 0.001) in all children.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endothelin (ET-1) is involved in the contrast media induced nephrotoxicity in children with congenital heart disease. 778 Nov 98

To determine whether circulating levels of endothelin-1 (ET-1), a potent vasoconstrictor peptide, are elevated in children with pulmonary hypertension and related to the degree of hypoxic pulmonary vasoconstriction, we measured arterial and mixed venous plasma concentrations of immunoreactive ET-1 (irET-1) in 13 children during cardiac catheterization. Clinical diagnoses in seven children with pulmonary hypertension (PH) included chronic lung disease (four children), congenital heart disease after surgical repair (two children), and primary ("reactive") pulmonary hypertension (one child). Blood samples were simultaneously obtained from pulmonary artery (venous) and systemic arterial sites during baseline conditions. Plasma irET-1 was elevated in children with PH (12.3 +/- 3.4 versus 3.6 +/- 0.7 pg/ml, PH versus non-PH; p < 0.01). Arterial/venous irET-1 ratios in the PH group (1.1 +/- 0.2) were not different from those in the non-PH group. During acute hypoxia, mean Ppa increased from 27 +/- 3 to 40 +/- 5 mm Hg. Basal irET-1 correlated strongly with the degree of elevation of mean Ppa during acute hypoxia (r = 0.69; p < 0.02). We conclude that irET-1 levels are often elevated in children with PH, and they are strongly correlated with pulmonary vasoreactivity during acute hypoxia. Whether elevated irET-1 levels contribute directly to or are markers of altered pulmonary vascular tone and reactivity in children with PH remains speculative.
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PMID:Circulating immunoreactive endothelin-1 in children with pulmonary hypertension. Association with acute hypoxic pulmonary vasoreactivity. 834 19

To investigate the regulation of endothelin-1 (ET-1) production, cardiac catheterization was performed in young patients with congenital heart disease (27 +/- 5 months old, mean +/- SEM), and plasma levels of ET-1 in the inferior vena cava were measured by a sandwich-enzyme immunoassay. Plasma ET-1 levels of age-matched healthy controls were 1.55 +/- 0.07 pg/ml (n = 6). In patients with atrial septal defect [without pulmonary hypertension (PH)] who had volume but not pressure overload to the pulmonary circulation (PC), plasma ET-1 levels were significantly lower than in controls. In patients with PH due to ventricular septal defect (VSD) who had both volume and pressure overload to PC, the levels were significantly higher than in controls. In patients with PH and severe pulmonary congestion due to pulmonary venous stenosis (PVS), plasma ET-1 levels were significantly higher than in those with VSD, suggesting that ET-1 production is also augmented by pulmonary congestion. The present findings suggest that ET-1 production is increased by pressure overload to PC but decreased by volume overload to PC.
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PMID:Influence of pulmonary blood pressure and flow on endothelin-1 production in humans. 858 35

We have previously reported that plasma endothelin-1 (ET-1) levels were significantly increased after exercise in healthy athletes. In the present study, venous plasma ET-1 levels were measured to investigate whether the role of ET-1 during exercise differs between healthy athletes and patients with congenital heart disease. Seven patients (mean age 13 years) performed symptom-limited treadmill exercise (Bruce protocol). All patients were in class I of the NYHA functional classification. The mean end-exercise O2 utilization was 32 ml/min/kg (166% of ventilatory threshold). Blood sampling was carried out in the seated position. The plasma ET-1 level was 1.21 pg/ml before exercise and did not alter immediately after or 30 min after exercise. The plasma level of norepinephrine was markedly elevated immediately after exercise and returned to the basal level 30 min after exercise. The present study demonstrated that exercise failed to alter plasma ET-1 levels in patients with congenital heart disease.
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PMID:Plasma endothelin-1 levels after exercise in patients with congenital heart disease. 858 55

This study applied bronchoalveolar lavage (BAL) to children with congenital heart disease (CHD) prior to elective cardiac catheterization (n = 48), to determine the influence of pulmonary blood flow and viral infection on the alveolar epithelial lining fluid (ELF) concentration of leucocytes, protein and endothelin-1 (ET-1). Lower respiratory tract (LRT) viral infection was defined as either a positive immunofluorescence for virus, or a virus cultured from the bronchoalveolar lavage fluid (BALF). Haemodynamic status was determined at cardiac catheterization. Normative data for BALF, but not ELF parameters, were obtained from 26 asymptomatic, noninfected normal children undergoing elective surgery. In the absence of LRT infection, the BALF macrophage, lymphocyte and neutrophil differential in CHD was not significantly different from the normal controls. In CHD, both increased pulmonary-to-systemic flow ratio (Q'p/Q's) and increased pulmonary artery-to-left ventricular pressure ratio PAP/LVP were associated with a decrease in ELF protein (rs = -0.59; p < 0.0001; and rs = -0.50; p < 0.0001 respectively). A respiratory virus was isolated from the BALF in 8 (17%) of CHD children. Virus isolation was associated with an increased ELF total protein (p < 0.05 vs no infection), a decreased alveolar macrophage differential count (p < 0.01), and an increased neutrophil differential count (p < 0.05). ET-1 was detected in the BALF of 83% of the noninfected CHD children compared to only 23% of the controls (p < 0.001). ELF ET-1 concentrations did not correlate with haemodynamic status in CHD, but were up to 100 times higher than paired plasma levels. We conclude that, in congenital heart disease, both lower respiratory tract viral infection and increased pulmonary blood flow and/or pulmonary vascular pressure influence the alveolar milieu. High alveolar epithelial lining fluid concentrations of endothelin-1 occur in congenital heart disease, but the stimulus for pulmonary endothelin-1 production is unclear.
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PMID:Alveolar epithelial lining fluid cellularity, protein and endothelin-1 in children with congenital heart disease. 883 47

Improved cardiovascular morbidity and mortality have been observed in several clinical studies of dietary supplementation with coenzyme Q10 (CoQ10). We elucidated the effect of CoQ10 on certain hemostatic parameters that may influence the progression of heart disease. Twelve Yorkshire swine were randomized to receive diet supplementation with either CoQ10 or placebo for 20 days. Blood samples were obtained at baseline and at the end of the feeding period. At the end of the protocol, there were no significant differences in hemostatic parameters in the placebo group. A significant increase in total serum CoQ10 level (from 0.39 +/- 0.06 to 0.96 +/- 0.04 microgram/ml, p < 0.001) was noted after the feeding period in the CoQ10-supplemented group. We observed significant inhibition of ADP-induced platelet aggregation (-9.9%) and a decrease in plasma fibronectin (-20.2%), thromboxane B2 (TXB2, -20.6%), prostacyclin (-23.2%), and endothelin-1 (ET-1, -17.9%) level. There were no changes in the plasma concentrations of the natural antithrombotics [antithrombin-III (AT-III), protein S, and protein C] after CoQ10 supplementation. CoQ10 supplementation in a dose of 200 mg daily is associated with mild antiaggregatory changes in the hemostatic profile. Clinical beneficial effects of CoQ10 may be related in part to a diminished incidence of thrombotic complications.
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PMID:Hemostatic changes after dietary coenzyme Q10 supplementation in swine. 885 71

A paracrine pathway for the regulation of cardiac contractile function by nonmuscle cells is documented in the heart. Coronary and endocardial endothelium release several diffusible agents, such as prostaglandins, endothelin-1, and nitric oxide, with an action on cardiac myocyte function. Cardiac diseases involving an immune or inflammatory mechanism, such as endotoxic shock, are now seen as conditions in which cross-talk between different cell types in the heart is clearly implicated. The potential biological relevance of inducible nitric oxide synthase in the myocardium, and the subsequent production of nitric oxide has been proposed as a mechanism of the cardiac depression observed in septic shock. In addition to cardiac myocytes, activated microvascular endothelial cells and cardiac endothelial cells may contribute to nitric oxide generation and, ultimately, to the depression of myocardial contractile activity during sepsis. This article reviews the local intercellular communication between cardiac myocytes and endothelial cells in the normal heart and discusses some of the mechanisms potentially claimed to depress heart function in sepsis.
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PMID:Paracrine regulation of cardiac myocytes in normal and septic heart. 955 26


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