Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

35 patients were treated for acute myeloid leukaemia or acute lymphoblastic leukaemia with allogeneic bone-marrow grafts from a parent, child, or sibling who was mismatched at the major histocompatibility complex (MHC). 11 of these patients are alive at least 6 months after grafting, 5 of them after more than 2 years. Of the 15 patients aged under 20 at the time of the graft, 8 are alive and well 6 months to 3 years later. Cyclosporin A was given to all patients after grafting. 1 patient died of acute graft-versus-host disease and in 2 other cases this was a major factor in their death. Graft failure caused the death of 2 patients. 4 patients died of recurrent leukaemia. A fatal complication in 12 patients was pulmonary oedema, often associated with convulsions, intravascular haemolysis, and renal failure. Some of these patients had viral or bacterial infections, but in the majority the syndrome was not associated with demonstrable infection. This syndrome, in which the essential lesion appears to be vascular, was much more common in recipients of mismatched than matched grafts. 3 others died from lung disease in which infection was a factor.
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PMID:Mismatched family donors for bone-marrow transplantation as treatment for acute leukaemia. 613

Neonatal hyaline-membrane disease is complicated by pulmonary edema, yet left atrial pressures are normal. Alveolar-capillary-membrane permeability may therefore be increased. To assess pulmonary epithelial permeability, we measured the pulmonary clearance and half-life of aerosolized 99mTc-diethylenetriamine pentacetate (99mTc-DTPA) on 31 occasions in 15 intubated premature infants with hyaline-membrane disease. Three infants with respiratory failure due to other diseases were studied on four occasions. All studies of infants with hyaline-membrane disease that were performed in the first 72 hours of life demonstrated a biphasic clearance curve with a rapid-phase half-life of 1.6 +/- 0.6 minutes (mean +/- S.D.). As these infants recovered, the curve became monophasic with a half-life of 56.0 +/- 32.1 minutes. Two infants remained dependent on oxygen and ventilator support and had persistent biphasic curves with a rapid-phase half-life of 1.5 +/- 0.7 minutes. All infants without hyaline-membrane disease had monophasic curves with a half-life of 65.4 +/- 33.6 minutes. Using a similar technique, we observed that newborn lambs and piglets have a monophasic pulmonary clearance of 99mTc-DTPA (114 +/- 59 minutes in lambs and 52.5 +/- 16.3 minutes in piglets). We conclude that the lungs of neonates with hyaline-membrane disease are abnormally permeable to small solutes and that this abnormality persists in infants with subsequent chronic lung disease.
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PMID:Pulmonary epithelial permeability in hyaline-membrane disease. 638 82

To evaluate the cardiac anatomy and functional hemodynamics in young infants with chronic lung disease, nine patients, aged 2 to 7 months, with a clinical diagnosis of bronchopulmonary dysplasia (BPD) underwent echocardiographic examination. All infants required supplemental O2 (mean FIO2 35%) to maintain adequate systemic oxygenation (Pao2 greater than 50 mm Hg). None of the infants had evidence of a patent ductus arteriosus at the time of examination. Echocardiographic measurements of left and right ventricular systolic time intervals revealed normal systolic time interval ratios suggesting pulmonary vascular resistances. However, echocardiographic evidence of left ventricular hypertrophy was found in eight of the nine infants, while right ventricular anterior wall thickness and right ventricular diastolic dimensions were not increased. Two infants died; marked left ventricular hypertrophy was noted at the time of postmortem examination while the right ventricular wall thickness was normal. The findings of left ventricular hypertrophy led to a retrospective review of autopsy material of seven patients who died with BPD over the past year. In six of seven cases examined, left ventricular posterior wall thickening was noted (range 7 to 11 mm); while the right ventricular wall thickness was normal (range 2 to 5 mm). These data suggest that (1) as assessed by echocardiography, the pulmonary vascular resistance is not significantly elevated in young infants with BPD, and (2) a hypertrophic left ventricle evolves which may assume importance in the pathogenesis of pulmonary edema in BPD, though the precise etiology remains undetermined.
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PMID:Normal pulmonary vascular resistance and left ventricular hypertrophy in young infants with bronchopulmonary dysplasia: an echocardiographic and pathologic study. 644 73

Pulmonary edema is an important feature of many newborn lung diseases, including respiratory distress from severe perinatal asphyxia, heart failure, hyaline membrane disease, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often results from increased filtration pressure in the microcirculation of the lungs. This occurs during sustained hypoxia, in left ventricular failure associated with congenital heart disease or myocardial dysfunction, following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution, and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema) or fibrosis (long-standing lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
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PMID:Edema formation in the lungs and its relationship to neonatal respiratory distress. 657 79

Lung sounds were recorded in three groups of 5 subjects, 2 conditions associated with pulmonary crackling (asbestosis and pulmonary oedema), and in normal non-smoking males. A technique was used which permitted extraction and analysis of the low-frequency sounds. Differences were evident in the 5-50 Hz range of the frequency spectra which allowed separation of all 3 groups. A prominent feature was the close similarity of the low-frequency sounds within the asbestos group when plotted on a scattergram. The findings suggest that alteration in low-frequency breath sound occurs in parenchymal lung disease and that its potential merits further investigation.
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PMID:Alteration in the low frequency lung sounds in respiratory disorders associated with crackles. 670 59

Pulmonary edema is an important cause of respiratory distress in newborn infants. It occurs with severe perinatal asphyxia, heart failure, hyaline membrane disease, persistent patency of the ductus arteriosus, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often develops from increased pressure in the microcirculation of the lungs. This may occur in conjunction with sustained hypoxia; left ventricular failure associated with congenital heart disease or myocardial dysfunction; following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema of fibrosis (chronic lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen-breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. Epithelial protein leaks may develop when the transpulmonary pressure needed to inflate the lungs increases because of high surface tension at the air-liquid interface. Fibrin clots from in some of the air spaces, which in combination with atelectasis and edema constitute the pathologic features of hyaline membrane disease. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen fluid filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
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PMID:Edema formation in the newborn lung. 676 Oct 39

A 37-year-old woman with a post-traumatic seizure disorder had four well-documented episodes of postictal acute pulmonary edema and respiratory failure. Subtherapeutic blood concentrations of phenytoin were documented on each admission. Each episode followed one or more grand mal seizures and was characterized by the development of diffuse nodular-appearing alveolar infiltrates, tachypnea, and severe hypoxemia that rapidly resolved with supportive therapy. There was no evidence of gastric acid aspiration, acute lung infection, or underlying heart or lung disease. To determine the frequency of postictal pulmonary edema in our institution, we reviewed the clinical records and chest roentgenograms of 45 consecutive patients who were admitted to our emergency room following a well-documented grand mal seizure. Only one patient (described in this report) had chest roentgenographic evidence of pulmonary edema. A review of the English literature revealed only 11 reported cases of postictal pulmonary edema since 1965 and a total of 42 episodes in 27 patients since 1908. There were no clearly documented cases of postical pulmonary edema following electroconvulsive therapy in 18 published reports totaling more than 38,000 subjects. Our findings suggest that while postictal pulmonary edema may occur repeatedly in the same patient, the overall frequency of this complication is low.
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PMID:Recurrent postictal pulmonary edema: a case report and review of the literature. 679 85

In order to establish a model of lung disease in which the usefulness of potential antiinflammatory compounds can be evaluated, we have analyzed the biochemical and cellular responses of rabbits to zymosan deposition in their lungs. A suspension of zymosan particles was instilled into the lungs of rabbits using an intratracheal catheter. Because the influx of leukocytes and the transudation of plasma into affected lungs was expected to contribute to the total cellular enzyme and protein levels, lungs were homogenized and assayed after various time intervals for six cellular enzymes and for protein content. After one day, alkaline phosphatase and neutral protease levels were elevated by 90% and 50%, respectively, above normal values. After two and three days, all of the pulmonary enzymes assayed displayed maximal two- to fourfold increases in their levels of activity. After seven days, only the alkaline phosphatase and neutral protease levels remained slightly elevated by 50% and 30%, respectively. Histologic analysis revealed focal and diffuse intraalveolar, interstitial, peribronchiolar, and perivascular accumulations of macrophages, granulocytes, and lymphocytes. Severe pulmonary edema, evident microscopically after one to three days, correlated well with 100% increases in both the wet weight and protein content of the lungs. In control experiments, the intratracheal infusion of saline solution minus zymosan particles resulted in a variety of enzymatic changes in the lungs after three days, which could be distinguished both enzymatically and histologically from those following zymosan deposition; histopathologic analysis revealed a pattern of intravascular congestion with erythrocytes, edematous thickening of alveolar septa, and focal intraalveolar hemorrhages, but with no inflammatory infiltration. In summary, this study demonstrates the time course of an experimental model for acute and chronic lung inflammation, the extent of which may be quantitatively evaluated using cellular enzymatic markers.
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PMID:Biochemical and morphologic changes in rabbit lung following endotracheal instillation of zymosan particles. 686 90

The recognition that inhaled nitric oxide (NO.) selectively vasodilates the pulmonary vasculature and the fact that pulmonary artery hypertension appears to play a pivotal and central role in the clinical manifestations of adult respiratory distress syndrome have led to an explosion of interest in this treatment modality. Improved pulmonary function and reduced ventilatory support have been noted in some patients with acute lung disease treated with inhaled NO.. The efficacy of inhaled NO. in various animal models has been inconsistent. Although it appears likely that inhaled NO. will be a useful adjunct in the treatment of patients with acute lung disease, the appropriate role of inhaled NO. in the treatment of ARDS remains uncertain. In order for inhaled NO. to be clinically useful in patients, this modality will have to be combined with other treatments that alter the florid inflammatory response. One should anticipate the most benefit in patients in whom respiratory failure is secondary to pressure-driven pulmonary edema and true intrapulmonary shunt.
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PMID:Inhaled nitric oxide in acute lung disease. 770 94

The so-called ground glass pulmonary opacity is characterized by a slight increase in lung density, with persistent visibility of vascular structures and bronchial walls. If vessels are obscured, the term consolidation is preferred. This kind of pulmonary opacity, which may be patchy or diffuse, was well known in conventional radiology, but has been recently re-evaluated, following the increasingly widespread use of high resolution CT of the lung. Ground glass opacity is commonly observed in patients with early diffuse pulmonary infiltrative diseases. Though non-specific in itself, the sign is always very significant. Particularly, it could represent a useful sign of active and treatable abnormality in some diffuse pulmonary diseases, such as idiopathic pulmonary fibrosis and sarcoidosis. The ground glass opacity may also be observed in pulmonary edema, desquamative pneumonitis, Pneumocystis carinii pneumonia, alveolar proteinosis, hypersensitive pneumonitis and drug induced or radiation induced lung disease. This paper represents a contribution to the understanding of the pathologic bases of the ground glass pulmonary opacity and an introduction to its differential diagnosis.
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PMID:[Diffuse ground-glass opacity of the lung. A guide to interpreting the high-resolution computed tomographic (HRCT) picture]. 782 71


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