Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alveolo-arterial difference in PO2 (AaDO2) during moderate hyperoxia (FIO2 = 0.40) and shunt-effect (Qs/Qt) were measured in 219 patients with chronic lung disease of various aetiologies. In particular, the series included 79 chronic bronchitics, 35 cases of "primary" emphysema, 40 cases of sarcoidosis and 36 cases of diffuse interstitial pulmonary fibrosis ( DIPF ). Alveolar PO2 was calculated from the equation of alveolar air. Ventilatory parameters were measured under stable conditions using a Fleisch metabograph . Shunt-effect (in moderate hyperoxia) was calculated from the classical equation. AaDO2 in chronic bronchitis was on average 118.3 +/- 30.7 mmHg, significantly higher (p less than 0.005) than in the emphysema patients: 99.2 +/- 22.3 mmHg. The same difference between the two groups was found for shunt-effect (p less than 0.005). In sarcoidosis, AaDO2 and Qs/Qt were only slightly raised on average: 83.6 +/- 22.0 mmHg and 7.2 +/- 3.7% respectively. By contrast, in DIPF , AaDO2 was very high (124.9 +/- 35.7 mmHg) as was Qs/Qt (14.8 +/- 6.9%). The measurement (in moderate hyperoxia) of AaDO2 and Qs/Qt, which are fairly representative of ventilation-perfusion inequalities, may thus make a contribution to the physiopathological differentiation between chronic bronchitis and emphysema. The frank increase in AaDO2 and Qs/Qt in DIPF emphasises the importance of ventilation-perfusion inequalities in the development of hypoxaemia in such patients. For all the cases studied, there was a very satisfactory correlation between AaDO2 in moderate hyperoxia and PaO2 at rest in ordinary air (r = -0.64, p less than 0.001). Similarly, there was a satisfactory correlation between Qs/Qt in moderate hyperoxia and PaO2 at rest in ordinary air (r = -0.53, p less than 0.01).
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PMID:[Value of the measurement of the alveolo-arterial PO2 difference in moderate hyperoxia (FIO2 = 0.40) in chronic respiratory insufficiency]. 672 46

Pulmonary surfactant, a complex of lipids and proteins, maintains alveolar integrity and participates in the control of host defense and inflammation in the lung. Surfactant proteins A, B, C, and D are important components of surfactant that play diverse roles in the surface tension reducing as well as host defense and inflammation control functions of surfactant. Hyperoxia or exposure of cells/tissues to elevated levels of oxygen occurs when high levels of oxygen are used to treat a variety of pulmonary disorders that include respiratory distress syndrome of premature infants, emphysema, sarcoidosis, end-stage lung diseases, and others. The lung serves as a primary target organ in hyperoxia, and hyperoxic lung injury is characterized by pulmonary edema, inflammation, and respiratory failure. Hyperoxic lung injury is associated with significant changes in the expression of surfactant proteins that likely serves as an adaptive response to elevated oxygen levels. In most animal species studied, hyperoxia increases the tissue expression of surfactant protein mRNAs. A limited number of studies have indicated that the increased tissue expression of surfactant protein mRNAs is associated with increased levels of surfactant proteins in the bronchoalveolar lavage.
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PMID:Regulation of surfactant protein gene expression by hyperoxia in the lung. 1471 50