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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of prostaglandin E1 on mean pulmonary artery pressure (Ppa):cardiac index (Q) relationships were investigated in eight anaesthetized dogs, ventilated in hyperoxia (fraction of inspired oxygen (FiO2) 0.4) and in hypoxia (FiO2 0.1). Cardiac output was increased by opening an arterio-venous femoral bypass or reduced by stepwise inflations of a balloon in the inferior vena cava. Five-point Ppa:Q relationships were found to be linear in all experimental conditions. Hypoxia increased Ppa over the entire range of Q studied (1-5l.min-1.m-2). Prostaglandin E1 0.4 microgram.kg-1.min-1 intravenously decreased hyperoxic Ppa for Q ranging from 3-5 l.min-1.m-2, hypoxic Ppa for Q ranging from 2-5 l.min-1.m-2 and attenuated hypoxia-induced increases in Ppa. These results show that prostaglandin E1 is a pulmonary vasodilator in both hyperoxic and hypoxic conditions. At the dose of 0.4 microgram.kg-1, prostaglandin E1 partially inhibits hypoxic pulmonary vasoconstriction.
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PMID:Pulmonary artery pressure--flow plots in hyperoxic and in hypoxic dogs: effects of prostaglandin E1. 314 79

Prostaglandin metabolism by rat lung tissue was measured following exposures of 6, 24 and 48 hours to either pure oxygen or air at one atmosphere. Tissue concentrations of PGE1, PGE2 and PGF2 alpha were not altered by oxygen exposures. Prostaglandin synthetase activity decreased between 24 and 48 hours but was not significantly different from control at 48 hours. Combined prostaglandin dehydrogenase/reductase activity decreased between 24 and 48 hours to 13% of control values and was significantly lower than in air at 48 hours. The plasma concentration of 13, 14 dihydro-15-keto PGF2 alpha, a catabolite of PGF2 alpha, was significantly lower in oxygen-exposed rats at 24 and 48 hours. We conclude that endogenous pulmonary prostaglandin concentrations are maintained during hyperoxia but that catabolism of prostaglandins by the lungs may be impaired.
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PMID:Pulmonary prostaglandin metabolism during normobaric hyperoxia. 626 Dec 83

Exposure to hypoxia (10% O2 for 5 to 7 days) results in increased survival and decreased pulmonary toxicity of adult rats subsequently exposed to hyperoxia (> 97% O2). These experiments tested whether hypoxia preexposure minimized the decrease in lung metabolism of prostaglandin E1 (PGE1), a vasoactive and antiinflammatory prostaglandin, caused by hyperoxia. Transpulmonary PGE1 clearance was measured as fractional metabolism of PGE1 (2 microM to 30 microM) infused during a 45-second period in an isolated, buffer-perfused rat lung preparation after exposure of rats to one of the following conditions: (1) hyperoxia (> 97% O2 for 48 hours), (2) hypoxia (10% O2 for 120 hours), or (3) hypoxia followed by hyperoxia. Hyperoxia exposure decreased both lung PGE1 metabolism and lung prostaglandin dehydrogenase activity (PGDH). Hypoxia also decreased lung PGE1 metabolism but, in contrast, increased lung PGDH activity. Hypoxia preexposure did not prevent the depression of PGE1 metabolism or PGDH activity caused by hyperoxia, which indicates that survival in hyperoxia did not depend on lung PGE1 metabolism. Hypoxia itself impaired transpulmonary metabolism of PGE1 despite increasing PGDH activity, which suggests possible interference with substrate delivery.
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PMID:Effects of hypoxia and hyperoxia on lung prostaglandin E1 metabolism. 907 31