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

A twofold increase in left ventricular output was achieved by suturing a Telfon graft between the aorta and left atrium in dogs. Three weeks after surgery the animals were anesthetized and found to have left ventricular end-diastolic pressures averaging 36 mmHg with markedly elevated right ventricular systolic pressures (RVSP). Oxygen breathing resulted in a decrease in left ventricular pressures, RVSP, and arterial pressure in those animals which survived hypoxia. Fifty percent of the shunted dogs subsequently developed fatal pulmonary edema when allowed to breathe 10% oxygen in nitrogen. These animals showed no change in left ventricular function or pulmonary artery pressure (RVSP) in response to pure oxygen administration. It is suggested that there is a gradation of hemodynamic response to pure oxygen depending on the severity of left ventricular overload. In the severest case the 'fixing' of pulmonary hypertension may be due to neurohumoral mechanisms. The subsequent development of pulmonary edema in these animals with hypoxia either involves a change in permeability or a redistribution of hydrostatic pressure within the pulmonary vasculature.
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PMID:The effects of changes in inspired oxygen concentration on the experimental production of pulmonary edema in the dog with chronic left ventricular overload. 2 12

Forty-three patients (mean age 62 +/- 1 years) were treated for ventricular septal defect (VSD) secondary to myocardial infarction. Whenever possible, operation was postponed until six weeks post-onset chest pain. However, hemodynamic instability, evidenced by cardiogenic shock, refractory pulmonary edema, or a rising blood urea nitrogen (BUN) forced operation in 21 patients within 21 days post-infarct (Group I). In seven patients operation was performed three to six weeks post-infarct (Group II). In only eight patients could operation be delayed beyond six weeks post-infarct (Group III). Clinical deterioration, once begun, progressed rapidly, and could be reversed only temporarily by intra-aortic balloon pumping, used in 26 patients for safe conduct of cardiac catheterization and for peri-operative hemodynamic support. Hospital survival was achieved in 24 of the 36 operated patients (66%). In Group I patients, ten of 21 survived. In Group II, six of seven survived. In Group III, eight of eight patients survived. There have been five late deaths with a mean follow-up of 41 months in survivors. Improved survival has been achieved recently by the greater use of prosthetic material to replace necrotic muscle and by a transinfarct incision regardless of infarct location. Operative mortality before 1973 was 47%; mortality after 1973 was only 18%, with a concomitant reduction of mortality (30%) even in Group I patients.
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PMID:Surgery for post-myocardial infarct ventricular septal defect. 30 10

A rhesus monkey (Macaca mulatta), accidentally exposed to vapors of methyl methacrylate for 22 hours was found in a comatose condition. Attempts to revive the animal were unsuccessful. Necropsy revealed a diffusely mottled liver, pulmonary edema, and atelectasis. The thoracic cavities each contained 30 ml of clear yellow fluid. Histopathologic review of the tissues showed central lobular liver necrosis, pulmonary edema, pulmonary emphysema, and atelectasis. Analysis of a blood sample obtained from the monkey 1.5 hours prior to death showed a normal hemogram, but elevated values for serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, lactate dehydrogenase, phosphohexose isomerase, blood urea nitrogen, and serum sodium. The pathologic findings, laboratory results, and clinical history suggested a diagnosis of methyl methacrylate poisoning.
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PMID:Accidental methyl methacrylate inhalation toxicity in a rhesus monkey (Macaca mulatta). 40 81

Nitrogen idoxide (NO2) is both edematogenic and cytotoxic to the lung. Preexposure to NO2 protects against mortality from formation of excessive pulmonary edema (tolerance) and, depending on the preexposure schedule, may or may not protect against the cytotoxic effects of NO2 in the lung. Measurement of DNA synthesis in hamster lung was used to study the question of whether the more subtle cytological injury induced by NO2 is mediated by a system which also exhibits tolerance. It was found that when hamsters are preexposured daily to 10 ppm NO2, they develop tolerance against normally lethal concentrations of NO2; are protected against further cytological injury from 10 ppmNO2; but are not protected from the cytotoxic effects of NO2 greater than 10 ppm. Animals exposed weekly to 10 ppm NO2 are not protected from further cytotological injury induced byweekly exposures to 10 ppm NO2, but do develop tolerance against lethal concentrations of NO2. Thus the data indicate that induction of tolerance to NO2 does not necessarily protect the cell populations of the lung from the cytotoxic effects of NO2.
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PMID:Stimulation of DNA synthesis in lungs of hamsters tolerant to nitrogen dioxide. 42 33

Serial physiologic studies were performed to characterize both the immediate and delayed effects of a single occupational exposure to nitrogen dioxide in a nonsmoker. During the initial acute stage of pulmonary edema, the abnormal static pressure-volume curve and decreased static compliance corresponded to a reduction in pulmonary volume. During the delayed acute stage, elastic recoil and properties of resistance to flow were normal, but dynamic compliance was reduced and dependent on respiratory frequency, and oxygen transport was abnormal during exercise, which is consistent with dysfunction of the small airways.
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PMID:Dysfunction of small airways following pulmonary injury due to nitrogen dioxide. 43 27

Twenty-three patients exposed to nitrogen dioxide in agriculture or industry were referred to the University of Wisconsin Medical Center. Eighteen experienced a transient upper respiratory tract syndrome; five developed pulmonary edema or bronchiolitis obliterans. This latter group responded to steroid therapy but all demonstrated evidence of persistent pulmonary dysfunction on follow-up studies. Combining our findings with those in the literature we concluded: (1) exposure to NO2 is more common than generally appreciated; (2) case fatality is high--29% for silo-filler's disease; (3) steroids are effective therapy and should be continued for at least eight weeks; (4) although the majority recover without significant sequelae, some individuals may develop persistent functional abnormalities; (5) there is no evidence that long-term exposure to low concentrations of NO2 leads to chronic airway obstruction; and, (6) NO2-induced pulmonary disease could be elminated with appropriate preventive measures.
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PMID:Nitrogen dioxide-induced pulmonary disease: five new cases and a review of the leterature. 62 25

The oxygen consumption of rat bronchioles suspended in a physiological salt solution containing plasma proteins was measured with the Cartesian diver microrespirometer. The oxygen consumption of the bronchiolar tissue 100-300 and 300-400 micrometer in diam was significantly (P greater than 0.01) reduced as the protein concentration of the suspending solution was increased from the low to the high extreme of the normal plasma physiological range and as the diffusion distance through the suspending medium was increased from 25 to 50 micrometer. The reduction in the bronchiolar oxygen consumption was significantly (P greater than 0.01) reversed by using 95% oxygen-5% nitrogen instead of air as the diffusing gas in the Cartesian diver. Measurements of the oxygen diffusivity in the protein solutions using a diaphragm diffusion cell showed a large decrease in the diffusivity as the plasma protein concentration was increased over the same concentration range used in the oxygen consumption studies. These results suggest that the reduction in oxygen consumption was secondary to a decrease in oxygen diffusion and may provide at least a partial explanation for the diffusion abnormalities which exist in noncardiogenic pulmonary edema in which there is an increase in microvascular membrane permeability to proteins.
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PMID:Inhibition of rat bronchiolar oxygen consumption by plasma proteins. 64 66

Unilateral pulmonary edema developed in a 48-year-old woman following intrapleural nitrogen mustard instillation. Despite progressive infiltration, the patient's symptoms resolved spontaneously.
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PMID:Unilateral pulmonary edema. An unusual complication of nitrogen mustard therapy. 93 42

We measured the protein composition of plasma and lung fluids from nine dogs with cardiogenic edema. To produce the edema, we increased left atrial pressure an average of 36 cmH2O by inflating a balloon catheter in the left atrium, infusing norepinephrine, and infusing large volumes of saline or saline-diluted blood. Blood samples were collected every 15 min, and airway fluid was collected from five dogs that developed severe edema. Terminally, the chest was opened and the lungs were removed. Samples of alveolar fluid were taken from the excised lung by direct pleural puncture with micropipettes. The lungs were frozen in liquid nitrogen and samples of free interstitial fluid were taken from the perivascular and peribronchial cuffs. Plasma and lung fluids were analyzed for total protein by the Lowry method and for albumin-globulin fractions by cellulose acetate electrophoresis. The average total protein concentrations (g/100 ml) were--plasma, 2.65; free interstitial fluid, 1.05; alveolar fluid, 1.23; and airway fluid, 1.29. The average albumin fraction of plasma was 0.40; of alveolar fluid, 0.43; and of airway fluid, 0.43. The protein concentrations in the three lung fluids were nearly identical to each other, but were less than half that of plasma. We conclude that in high-pressure pulmonary edema with alveolar flooding, the capillary endothelium retains the ability to restrict protein relative to fluid filtration, but the alveolar epithelium becomes freely permeable to protein.
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PMID:Protein composition of lung fluids in anesthetized dogs with acute cardiogenic edema. 99 90

The effects of oxides of nitrogen inhalation are reported in a 21-year-old gardener exposed to silage gas. Initial nausea, cough and fever remitted, but respiratory failure developed 3 weeks later. Roentgenograms and lung function studies revealed pulmonary edema, volume restriction, and severely impaired gas exchange. Needle biopsy showed a nonspecific interstitial pneumonia. With steroid therapy all functional parameters except diffusing capacity returned to normal. Failure to inquire about non-occupational activities led to delayed diagnosis. A brief review of toxic effects of nitrogen oxides is presented.
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PMID:Silo-Filler's disease. 111 73


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