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

The treatment of nitrogen dioxide (NO2)-induced lung edema is controversial. In addition, mechanisms and patterns of interstitial edema formation in this form of increased permeability edema are unclear. To ascertain if methylprednisolone (MP) is effective in the therapy of NO2-induced edema, we exposed 108 unaesthetized guinea pigs, in groups of 12, to 277-448 ppm.hr NO2: in 60, we administered MP just before, and in 48 immediately after exposure. In each group, half the animals were randomly assigned to receive 30 mg/kg MP ip, and the other half saline. Mortality rates and lung water with wet weight/dry weight (W/D) ratios were calculated. Alveolar edema, periarterial interstitial edema, and NO2-induced bronchiolitis were graded semiquantitatively by light microscopy from freeze-substituted middle (ML) and lower lobes (LL). We found NO2 produced an exposure-dependent increase in lung water (R = 0.70, p less than 0.01). Treatment with MP preexposure produced a fourfold reduction mortality, and and a significant fall in W/D ratios and in alveolar and interstitial edema. No difference in the degree of acute bronchiolitis was found between treated and untreated animals, although ML had significantly more inflammation than LL. Treatment with MP immediately after NO2 was ineffective since mortality rates, W/D ratios, and alveolar and interstitial edema were not lower in the treated animals; there was significantly more intestitial edema in the middle lobes of the latter. Both LL and ML had equally abundant alveolar edema, but LL had significantly more interstitial edema, supporting our previous findings that in NO2-induced edema interstitial fluid accumulation follows alveolar flooding, with interlobar discrepancies probably due to differences in lung volume or in ventilation.
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PMID:Effect of methylprednisolone on nitrogen dioxide (NO2)-induced pulmonary edema in guinea pigs. 249 89

The acute inhalation LC50 of oxalyl chloride was determined in rats following a one-hour exposure. Four groups of 10 animals per group were exposed to a concentration range of 462-2233 ppm. One set of six animals was exposed to a concentration of oxalyl chloride of 1232 ppm for one hour to evaluate the histopathological change to the lungs. The LC50 is 1840 ppm with the 95% confidence interval between 1531 ppm and 2210 ppm. Microscopically, the lungs from the treated animals exhibited acute bronchiolitis, exudate within the alveoli, and congestion. Pulmonary edema appears to contribute significantly to mortality produced by oxalyl chloride. A comparison of the acute one-hour LC50 of oxalyl chloride to that of hydrogen chloride, phosgene, phosphorus oxychloride, boron trichloride, and chlorine indicates that it shares a comparable degree of acute toxicity to hydrogen chloride and is significantly less toxic via inhalation than the latter four chemicals.
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PMID:Acute inhalation toxicology of oxalyl chloride. 787 5