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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Perfusate composition may alter pulmonary hemodynamics and edema formation in perfused lungs. Perfusion for 3 h with Krebs-Henseleit solution with 3% bovine serum albumin did not produce pulmonary hypertension, pulmonary edema (assessed by lung wet-to-dry wt ratio), or increased macromolecular permeability (assessed by 125I-albumin uptake). Addition of blood to hematocrit levels of 10 or 20% resulted in pulmonary hypertension during the final hour of perfusion but not pulmonary edema or increased macromolecular permeability. Pulmonary hypertension during blood perfusion was primarily due to increased precapillary resistance. Perfusion with buffer solution without albumin produced edema and increased macromolecular permeability but not pulmonary hypertension. In lungs perfused with blood (20% hematocrit), thromboxane B2 levels increased in parallel with the pulmonary hypertension, and inhibition of cyclooxygenase or thromboxane synthase with indomethacin or dazmegrel prevented pulmonary hypertension. Perfusion with leukopenic blood (from prior nitrogen mustard administration or from filtration) also prevented pulmonary hypertension. We conclude that blood perfusion produces pulmonary hypertension via thromboxane A2 generation, which depends on leukocyte activation, and that perfusion with buffer solutions without albumin produces edema and increased permeability without pulmonary hypertension.
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PMID:Effect of blood and albumin on pulmonary hypertension and edema in perfused rabbit lungs. 775 18

A 32 year old man was admitted for dyspnea, hemoptysis, macroscopic hematuria, hypertension (140/100), peripheral edema and hemodynamic decompensation. Lung Xrays revealed pulmonary edema and a cavity in the left apex. Laboratory determinations revealed an altered renal function with increased creatinine and urea levels and nephrotic syndrome. There was leucocyturia, hematuria and cylindruria. The sputum showed a large number of acid-fast bacilli. The patient began anti-tuberculosis treatment with three drugs (isoniacid, rifampicin, pirazinamide). On ultrasonography, both kidneys revealed ecogenic lesions with size, shape and cortico-medular relationship preserved. The patient persisted with altered renal function, steady levels of urea nitrogen, creatinine and potassium, preserved diuresis and hypertension. Bidimensional echocardiogram: LVDD 55 mm, hypoquinetic septum, pericardic effusion, thickened pericardium, pleural effusion, shortening fraction decreased. He received treatment for this congestive cardiac failure and hypertension with enalapril, nifedipine and fursemide. A percutaneous renal biopsy was performed with anatomopathologic diagnosis of diffuse encocapillar proliferative glomerulonephritis with crescents (15%) and total glomerular sclerosis (33%). Immunofluorescence: positive, immune-complexes with IgM and C3. The patient gradually recovered his normal renal function, improved his pleural effusions and normalized his cardiac function. He was discharged in good clinical condition on the 69th day of anti-tuberculosis treatment. An association between pulmonary tuberculosis and glomerulonephritis is discussed. It is proposed that renal lesions might be the consequence of the tuberculosis due to the sedimentation of circulating immune-complexes.
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PMID:[Immune complex glomerulonephritis associated with pulmonary tuberculosis]. 785 90

Human inhalation exposures to relatively high mass concentrations of the oxidant gas nitrogen dioxide (NO2) can result in a variety of pulmonary disorders, including life-threatening pulmonary edema, pneumonia, and bronchiolitis obliterans. Inasmuch as most experimental studies to date have examined NO2-induced lung injury following exposures to near ambient or supra-ambient concentrations of NO2, e.g., < or = 50 ppm, little detailed information about the pulmonary injurious responses following the acute inhalation of higher NO2 concentrations that are more commensurate with some actual human exposure conditions is currently available. Described in this report are the results from a series of investigations in which various aspects of the inhalation toxicity of high concentrations of NO2 have been examined in laboratory rats. In the first component of our study, we characterized the kinetic course of development of lung injury following acute exposures to high concentrations of NO2 delivered over varying durations, and we assessed the relative importance of NO2 exposure concentration versus exposure time in producing lung injury. For a given exposure duration, the resulting severity of lung injury was found to generally scale proportionately with inhaled mass concentration, whereas for a given concentration of inhaled NO2, the magnitude of resulting injury was not directly proportional to exposure duration. Moreover, evidence was obtained that indicated exposure concentration is more important than exposure time when high concentrations of NO2 are inhaled. In a second component of our investigation, we assessed the pulmonary injurious response that occurs when NO2 is inhaled during very brief, 'high burst' exposures to very high concentrations of NO2. Such exposures resulted in significant lung injury, with the magnitude of such injury being directly proportional to exposure concentration. Comparisons of results obtained from this and the first component studies additionally revealed that brief exposures to the very high concentrations of NO2 are more hazardous than longer duration exposures to lower concentrations. In a third study series, we examined pre-exposure, exposure, and post-exposure modifiers of NO2-induced lung injury, including dietary taurine, minute ventilation, and post-exposure exercise. Results from these studies indicated: (i) dietary taurine does not protect the rat lung against high concentration NO2 exposure, (ii) the severity of acute lung injury in response to NO2 inhalation is increased by an increase in minute ventilation during exposure, and (iii) the performance of exercise after NO2 exposure can significantly enhance the injurious response to NO2.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Lung injury following exposure of rats to relatively high mass concentrations of nitrogen dioxide. 802 31

Oxides of nitrogen (NOx) are a ubiquitous group of air pollutants found in outdoor air as well as indoor environments. The main source of these contaminants is from the combustion of biofuel. Low level and chronic exposure occurs mainly in indoor environments. Acute and high level exposure can occur in a variety of industrial, agricultural, mining, and military settings. The adverse effect of chronic and low level exposure on lung function has been suggested by several epidemiologic studies. However, the results of controlled human exposure to ambient concentrations of NOx have been inconsistent. On the other hand, acute exposure to high levels of NOx has a relatively predictable clinical response in the form of airway irritation, development of pulmonary edema and, in some cases chronic airway disease. There are several lines of evidence to support the role of nutritional antioxidants in amelioration of oxidant lung damage induced by NOx.
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PMID:Human exposure to oxides of nitrogen at ambient and supra-ambient concentrations. 802 33

The prognostic value of exercise peak VO2 is still controversial. We therefore prospectively studied 75 patients in New York Heart Association functional class II or III with chronic heart failure stabilized by drug treatment. The patients (mean age of 58 +/- 10 years) were submitted to a clinical examination, a radionuclide determination of left ventricular ejection fraction, and a haemodynamic study at rest (right side catheterization); their plasma sodium, plasma creatinine and blood urea nitrogen levels were measured in addition to exercise peak VO2. An exercise peak VO2 threshold value of 14 ml.kg-1.min-1 was used to define two groups: GI (23 patients), with an exercise peak VO2 < or = 14 ml.kg-1.min-1 and G2 (52 patients) with an exercise peak VO2 > 14 m.kg-1.min-1. G1 and G2 were comparable in terms of age, heart rate, left ventricular ejection fraction, cardiac index and mean arterial pressure. Apart from exercise peak VO2, G1 and G2 also showed differences in right and left ventricular filling pressures, plasma sodium, plasma creatinine, blood urea nitrogen levels and exercise duration (all P < 0.01). Moreover the prognosis was worse in G1 than in G2: nine deaths vs 0, and seven major events--major events being defined as pulmonary oedema, hospitalization for heart failure, or severe ventricular arrhythmias--vs three (P < 0.001). A sub-group analysis (deceased patients, living patients with and without major events) was performed. Out of 20 clinical and paraclinical parameters, exercise peak VO2 proved to have the greatest prognostic value.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Exercise peak VO2 determination in chronic heart failure: is it still of value? 807 Apr 76

The following study was performed to determine the effects of phosphodiesterase IV (PDE-IV) inhibition and its attenuation of tumor necrosis factor (TNF alpha) production in a rat model of the Adult Respiratory Distress Syndrome (ARDS). Rats were either unexposed (n = 8), pretreated orally with vehicle prior to intratracheal saline exposure (n = 11), pretreated with vehicle prior to 7 mg/kg intratracheal endotoxin (LPS) administration (n = 22), or pretreated with 5 or 50 mg/kg rolipram prior to LPS exposure (n = 6 and 7, respectively). Blood was sampled 1 and 3 hr post LPS exposure and assayed for plasma TNF alpha concentrations. Twenty-four hours after LPS exposure, blood was sampled again for hematologic measurements. The rats were then anesthetized and exsanguinated. Bronchoalveolar lavage (BAL) was performed after the lung of each rat was removed and weighed. Rolipram pretreatment was protective against LPS-induced mortality and also resulted in reduced plasma TNF alpha concentrations. LPS induced pulmonary edema, as indicated by wet/dry lung weight ratio (W/D) and total BAL protein content (TP) was attenuated by rolipram pretreatment. LPS-induced alveolar hemorrhage was reduced by rolipram pretreatment, but LPS-induced pulmonary neutrophilia was not. The hemoconcentration induced by LPS was reduced by rolipram, as was the LPS-induced thrombocytopenia. However, LPS-induced changes in circulating leukocyte populations were actually exacerbated by rolipram. LPS-induced alterations in renal and hepatic function, indicated by increased blood urea nitrogen (BUN), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), were inhibited by rolipram.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Therapeutic intervention in a rat model of ARDS: IV. Phosphodiesterase IV inhibition. 838 94

The pulmonary donor pool would increase substantially if lungs could be safely transplanted after cessation of circulation. To determine whether ventilation of cadaver lungs could improve graft function, canine donors were sacrificed and then ventilated with 100% oxygen (n = 6) or 100% nitrogen (n = 6); 6 served as nonventilated controls. Four hours after death, the lungs were flushed with modified Euro-Collins solution and harvested. Controls were ventilated with 100% oxygen only during flush and harvest. Recipients were rendered dependent on the transplanted lung by occlusion of the right pulmonary artery and bronchus 1 hour after transplantation. Ventilation was maintained at a constant inspired oxygen fraction of 0.4. Four controls died of pulmonary edema shortly after occlusion of the native lung. The mean arterial oxygen tensions in the oxygen-ventilated, nitrogen-ventilated, and control groups at the end of 8 hours were 81 mm Hg (n = 4), 88 mm Hg (n = 3), and 55 mm Hg (n = 2), respectively. Postmortem oxygen ventilation improved early recipient survival and gas exchange. Postmortem nitrogen ventilation improved early gas exchange and delayed recipient death compared with non-ventilated controls. The mechanics of ventilation appears to confer a functional advantage independent of a continued supply of oxygen. Transplantation of lungs harvested from cadavers after cessation of circulation might be feasible.
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PMID:Cadaver lung donors: effect of preharvest ventilation on graft function. 849 30

Aflatoxin (AF)-contaminated and fumonisin B1 (FB1)-contaminated (culture material from Fusarium moniliforme) diets were fed singly and in combination to growing cross-bred barrows. Six barrows (3 replicates of 2 each; mean body weight, 17.5 kg) per group were fed: 0 mg of AF and 0 mg of FB1/kg of feed (control); 2.5 mg of AF/kg of feed; 100 mg of FB1/kg of feed; or 2.5 mg of AF plus 100 mg of FB1/kg of feed for 35 days. The effects on production performance, serum biochemical, hematologic, immunologic, and pathologic measurements were evaluated. Body weight, gain, and feed consumption were significantly (P < 0.05) decreased by AF and AF plus FB1 diets. The FB1 diet decreased feed consumption, and although body weight was numerically decreased, it was not statistically significant. Aflatoxin increased serum gamma-glutamyltransferase (GGT) activity and total iron concentration and decreased urea nitrogen concentration and unsaturated iron-binding capacity. The FB1-alone diet increased serum GGT activity, whereas the AF plus FB1 diet increased serum aspartate transaminase, cholinesterase, alkaline phosphatase, and GGT activities, increased RBC count, triglycerides, and total iron concentrations, and decreased unsaturated iron-binding capacity and urea nitrogen concentration. For the most part, the effects of the AF plus FB1 diet on body weight and hematologic measurements could be considered additive. However, the effect of the AF plus FB1 diet on cholinesterase and alkaline phosphatase activities was greater than additive and was a synergistic response. One pig in the FB1-diet group and 2 pigs in the combination-diet group died. Postmortem lesions in pigs of the FB1-diet group consisted of ascites and increased liver weight. Observations at necropsy for pigs of the AF plus FB1-diet group consisted of hydrothorax, ascites, pulmonary edema, gastric erosions and ulceration, and increased liver and spleen weights. The AF diet increased relative liver weight and resulted in liver that was pale, rubbery, and resistant to cutting. Histologic lesions consisted of hepatic necrosis or degeneration, or both, with variable degrees of bile duct proliferation in barrows of the AF-diet groups. Renal tubular nephrosis was observed in barrows of the FB1-diet group, but this was not consistent in the AF plus FB1-diet group. Cell-mediated immunity, as measured by mitogen-induced lymphoblastogenic stimulation index, was decreased in barrows of the AF and FB1-diet groups, and values in barrows given the combination diet were significantly decreased from those in barrows given the single toxin diets. It was concluded that AF and FB1 (from culture material), singly or in combination, can adversely affect clinical performance, serum biochemical, hematologic, and immunologic values and induce lesions in growing barrows. For most of the variables we evaluated under our study conditions and dosages of toxins, measurements were affected more by the combination diet than by either single toxin diet, and the toxic responses could be described as additive or more than additive, particularly for induction of liver disease.
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PMID:Influence of aflatoxin and fumonisin B1-containing culture material on growing barrows. 859 31

The content of lipids and fatty acids was measured in lung tissue of intact rats and animals with lung edema caused by nitrogen oxide or adrenaline. Lung edema was found to involve disagreement between the phospholipid and fatty acid spectra and to increase the permeability of membranes. The toxic and adrenaline-induced edemas were found identical as regards the type of changes in the ratio of fractions of neutral lipids, phospholipids, and fatty acid spectrum, that is, these shifts represent a nonspecific reaction of lung tissue to aggression.
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PMID:[Changes in the lipid spectrum of the lungs in poisoning by nitrogen oxides or adrenaline]. 866 4

Previous reports have shown that neutrophils are retained in the lung after acute embolization and that these neutrophils play an important role in the subsequent formation of permeability pulmonary edema. The present study was designed to test the hypothesis that acute embolic injury results in microvascular damage in lung regions with the greater retention of neutrophils. Seventeen pigs (20 +/- 2 kg) were embolized by injecting polystyrene beads (250 microns; labeled with 131I) into the right atrium over 5 min. Five pigs, which received no embolic beads, served as controls. Neutrophils (89 +/- 5% pure), isolated on Ficoll-Histopaque gradient, were radiolabeled with 111In-oxine. Twenty minutes after embolization, the radiolabeled neutrophils were injected into the right atrium along with 85Sr-labeled microspheres to mark the initial neutrophil distribution within the lung as well as the regional pulmonary blood flow at the time of their delivery. The animals were killed 50 min after embolization, and the lungs were removed, frozen over liquid nitrogen, and cut into 60 samples. The data show that after embolization regional neutrophil retention was inversely related to the regional blood flow but was not affected by the embolic load in the same region. Regional extravascular lung water was increased in regions of higher neutrophil retention, but the regions with increased edema did not receive a greater embolic load. These results show that microvascular injury occurs in the lung regions with the greatest neutrophil retention and that this increased retention of neutrophils is unrelated to the extent of embolization.
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PMID:Lung water is increased in regions of higher neutrophil retention after acute bead embolization. 872 34


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