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 antioxidant enzyme superoxide dismutase (SOD) found in the cytosol of eucaryotic cells and the plasma protein ceruloplasmin are copper containing proteins though to be important in providing protection from oxygen toxicity. To investigate the hypothesis that copper deficiency in the rat could result in decreased lung SOD activity and plasma ceruloplasmin concentration resulting in increased susceptibility to O2 lung damage, we performed a series of experiments exposing copper-deficient and control rats to normobaric and hyperbaric hyperoxia. Lung SOD activity in the copper-deficient rats was found to be 56% of control and ceruloplasmin content was 6% of control. The copper-deficient rats exhibited increased mortality and enhanced pulmonary toxicity as evidenced by increased pathologic damage and lung edema during the normobaric exposure to 85% O2. Copper-deficient animals also showed increased susceptibility to a hyperbaric exposure of 4 ata of 100% O2 with a decreased time of survival. The copper-deficient rat represents a new model for the study of oxidant injury.
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PMID:Enhanced pulmonary toxicity in copper-deficient rats exposed to hyperoxia. 672 91

Bronchopulmonary dysplasia is a most frequent contemporary lesion of the lung in early childhood. It is characterized by clinical symptoms (neonatal respiratory distress syndrome) and by X-ray picture reflecting progressive morphological changes in the respiratory tract, i.e. in trachea, bronchi, bronchioles, and pulmonary acini, followed by interstitial pulmonary lesion. As usual, bronchopulmonary dysplasia is forerun by hyaline membranes and may be associated with or followed by interstitial emphysema. Pathogenetic participants are toxicity of highly concentrated and long administered oxygen, artificial mechanical ventilation with an intermittently positive pressure, barotrauma first of immature lung causing emphysema and pneumothorax and pneumomediastinum, lung edema, shortage of A and E vitamins and ceruloplasmin deficiency. Morphological changes in bronchopulmonary dysplasia are alike diffuse alveolar damage in bigger children or adults. Nevertheless, neonatal changes differ from later pulmonary lesion by evolving in an immature tissue and by being complicated with necrotizing "obstructive" bronchiolitis.
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PMID:[Bronchopulmonary dysplasia]. 833 23