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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 vascular response to the inhalation of various concentrations of oxygen (FIO2) was studied under basal conditions and after nicardipine in 10 patients with pulmonary hypertension secondary to chronic bronchitis. Hemodynamic data and blood gases were measured during inhalation of 3 gas mixtures: hypoxia (FIO2 = 0.15), normoxia (FIO2 = 0.21) and hyperoxia (FIO2 = 0.30). Each gas mixture was administered for 20 minutes, initially during an infusion of placebo and then of nicardipine giving a steady plasma concentration of 29 +/- 4 ng/ml. This was obtained by continuous I.V. infusion of 0.06 mg/kg/hour. Under basal conditions with placebo, the heart rate, cardiac output and pulmonary hypertension increased with decreasing concentrations of inhaled oxygen. The systemic blood pressure was unchanged with hypoxia but decreased during hyperoxia. Nicardipine increased the heart rate and the cardiac output but reduced the blood pressure with every inhaled oxygen mixture. The blood pressure was independent of FIO2 and the reduction observed during hyperoxia with placebo no longer occurred with nicardipine. However, the pulmonary hypertension was unaffected. At the dosage used in this study, nicardipine modified the systemic vascular response to oxygen but not the pulmonary vascular response. The vasodilation induced was much greater in the systemic than in the pulmonary circulation. In relation to the absence of significant pulmonary vasodilation, no changes in blood gases, due to a possible pulmonary shunting effect, were observed. At this dosage, nicardipine is ineffective in reducing pulmonary hypertension. However, its systemic hypotensive action may be used in patients with respiratory failure due to chronic bronchitis without deleterious effects on blood gases.
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PMID:[Acute effects of nicardipine on the vascular reactivity of oxygen in patients with respiratory insufficiency and pulmonary hypertension]. 827 62

Chronic inflammation predisposes toward many types of cancer. Chronic bronchitis and asthma, for example, heighten the risk of lung cancer. Exactly which inflammatory mediators (e.g., oxidant species and growth factors) and lung wound repair processes (e.g., proangiogenic factors) enhance pulmonary neoplastic development is not clear. One approach to uncover the most relevant biochemical and physiological pathways is to identify genes underlying susceptibilities to inflammation and to cancer development at the same anatomic site. Mice develop lung adenocarcinomas similar in histology, molecular characteristics, and histogenesis to this most common human lung cancer subtype. Over two dozen loci, called Pas or pulmonary adenoma susceptibility, Par or pulmonary adenoma resistance, and Sluc or susceptibility to lung cancer genes, regulate differential lung tumor susceptibility among inbred mouse strains as assigned by QTL (quantitative trait locus) mapping. Chromosomal sites that determine responsiveness to proinflammatory pneumotoxicants such as ozone (O3), particulates, and hyperoxia have also been mapped in mice. For example, susceptibility QTLs have been identified on chromosomes 17 and 11 for O3-induced inflammation (Inf1, Inf2), O3-induced acute lung injury (Aliq3, Aliq1), and sulfate-associated particulates. Sites within the human and mouse genomes for asthma and COPD phenotypes have also been delineated. It is of great interest that several susceptibility loci for mouse lung neoplasia also contain susceptibility genes for toxicant-induced lung injury and inflammation and are homologous to several human asthma loci. These QTLs are described herein, candidate genes are suggested within these sites, and experimental evidence that inflammation enhances lung tumor development is provided.
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PMID:Susceptibility to neoplastic and non-neoplastic pulmonary diseases in mice: genetic similarities. 1535 60