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)

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

To ascertain whether the pattern of fluid accumulation could be altered by an agent introduced through the airways, the authors studied the physiology and morphology of 11 dogs exposed to 150-494 ppm.hr NO2 and compared them with 3 new and 5 previously reported control dogs. NO2 caused a partly reversible decrease in systemic arterial pressure and cardiac output, a fall in arterial PO2, and rapid shallow breathing, while pulmonary arterial and wedge pressures remained normal. Post mortem, lower (LL) and middle (ML) lobes were frozen, sections fixed for light microscopy by freeze-substitution, and wet weight/dry weight (W/D) ratios were measured. Alveolar edema was graded, and the distribution of interstitial edema around arteries and veins and within bronchovascular bundles was studied with morphometry: edema ratios (ER) were calculated as area of interstitium/area of vessel or airway. We found that NO2 produced an exposure-dependent increase in lung water (r = 0.73), and that both LL and ML had similar W/D ratios (7.77 and 8.39, respectively) and percent alveolar edema (30% and 34%). Morphometry of interstitial edema showed that the ER for vessels and airways of edematous LL were essentially similar to controls, while those of the ML were markedly increased. It is concluded that NO2 produces exposure-related lung edema and preferential alveolar flooding with probable secondary interstitial accumulation. The discrepancies in interstitial edema between middle and lower lobes may be due to differences in lung volume or in ventilation.
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PMID:Pattern of fluid accumulation in NO2-induced pulmonary edema in dogs. A morphometric study. 333 6

We had observed that very few Ladakhi soldiers (native highlanders: NHL) are hospitalized for high altitude pulmonary oedema. We hypothesized that this may happen because pulmonary artery pressures of NHLs do not increase even after exposure to acute hypoxia. The aim of this study was to test the above hypothesis by non-invasive echocardiographic assessment of pulmonary arterial pressure in freshly inducted Ladakhi soldiers and comparing it with that in freshly inducted lowlander soldiers (LL). The pre-ejection period and acceleration time ratio as measured from the pulmonary artery Doppler signal was used to compute mean pulmonary arterial pressure. In NHL this pressure on day 1 of induction was significantly lower at 25.8 +/- 6.5 mmHg as compared to 31.9 +/- 9.5 mmHg in LL (P = 0.0002). Another finding of interest was the very low Lake Louise acute mountain sickness score in the NHL (0.278 +/- 0.461 on day 2). This appears to be further evidence that the natives of Ladakh are adapted to hypoxia and not merely acclimatized.
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PMID:Pulmonary artery pressure in Ladakhi men on exposure to acute hypoxia after a stay at sea level. 1564 4

Hypoxemia is usually associated with acute mountain sickness (AMS), but most studies have varied in time and magnitude of altitude exposure, exercise, diet, environmental conditions, and severity of pulmonary edema. We wished to determine whether hypoxemia occurred early in subjects who developed subsequent AMS while resting at a simulated altitude of 426 mmHg (approximately 16,000 ft or 4880 m). Exposures of 51 men and women were carried out for 8 to 12 h. AMS was determined by Lake Louise (LL) and AMS-C scores near the end of exposure, with spirometry and gas exchange measured the day before (C) and after 1 (A1), 6 (A6), and last (A12) h at simulated altitude and arterial blood at C, A1, and A12. Responses of 16 subjects having the lowest AMS scores (nonAMS: mean LL=1.0, range=0-2.5) were compared with the 16 having the highest scores (+AMS: mean LL=7.4, range=5-11). Total and alveolar ventilation responses to altitude were not different between groups. +AMS had significantly lower PaO2 (4.6 mmHg) and SaO2 (4.8%) at A1 and 3.3 mmHg and 3.1% at A12. Spirometry changes were similar at A1, but at A6 and A12 reduced vital capacity (VC) and increased breathing frequency suggested interstitial pulmonary edema in +AMS. The early hypoxemia in +AMS appears to be the result of diffusion impairment or venous admixture, perhaps due to a unique autonomic response affecting pulmonary perfusion. Early hypoxemia may be useful to predict AMS susceptibility.
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PMID:Hypoxemia and acute mountain sickness: which comes first? 1911 10