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

This study evaluated the effect of hyperoxia on the pharmacokinetic function of the lung. Hyperoxia is known to disrupt the activities of the pulmonary prostaglandin dehydrogenase/reductase and angiotensin converting enzymes. This would be predicted to alter the activation/deactivation of prostaglandins or angiotensin. The ability of these enzyme systems to act upon these compounds was evaluated by measuring the changes in the peripheral vascular responses to exogenous prostaglandin and angiotensin. Two groups of conscious, chronically catheterized rabbits, one exposed to ambient air and the other to greater than 98% oxygen, were given bolus injections of angiotensin I, angiotensin II, prostaglandin E2, sodium nitroprusside, and phenylephrine before and during up to 88 h of air or oxygen exposure. The hyperoxic animals' responsiveness to angiotensin I and angiotensin II decreased by 47% and 55%, respectively, after 72 h of oxygen exposure. The hyperoxic animals demonstrated a 54% increase in the vasodilatory response to arterial prostaglandin E2. Normoxic rabbits demonstrated no changes in response to any of the compounds tested. These data indicate that chronic hyperoxia influences either the synthesis/degradation and/or vascular receptors to both angiotensin I and II and prostaglandins.
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PMID:Effects of chronic hyperoxia on the cardiovascular responses to vasoactive compounds in the rabbit. 316 78

Hyperoxia has been shown to disrupt certain membrane bound enzyme systems within the pulmonary endothelium which are responsible for the metabolism of several endogenous vasoactive compounds. This study was to evaluate whether the potential disruption of the prostaglandin dehydrogenase/reductase and angiotensin converting enzymes, as a consequence of hyperoxia, would alter the activation/deactivation of prostaglandins or the angiotensins (I and II) and thereby alter their peripheral cardiovascular actions. Two groups of anesthetized dogs, one group ventilated with ambient air and the other with 100% oxygen, were given bolus injections of angiotensin I, angiotensin II, prostaglandin E2, sodium nitroprusside, and phenylephrine before and during 8 h of exposure to air or oxygen. The hyperoxic animals demonstrated a significant increase in mean arterial pressure responsiveness to both angiotensin I and angiotensin II. The responsiveness to the drugs increased by 41% for angiotensin I and 43% for angiotensin II. The ambient air control dogs showed no significant changes for any compounds tested. These data indicate that with 8 h of hyperoxia the renin-angiotensin system's ability to influence cardiovascular function is augmented, whereas, the hemodynamic effects of prostaglandins are unaltered.
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PMID:Effects of 100 percent oxygen on the cardiovascular responses to vasoactive compounds in the dog. 386 38

Weanling male rats were fed semi-purified diets supplemented with 0, 60, or 600 IU X g-1 vitamin E or 0, 100 or 1000 ppb selenium. One group was injected daily with vitamin E at a rate equivalent to consumption of 60 IU X kg-1. Animals from all groups were sacrificed after exposure to normobaric oxygen or air for 48 h. Lung tissue was analyzed for the combined activity of prostaglandin dehydrogenase and reductase. Using the decline in enzyme activity as an indicator of susceptibility to oxygen poisoning, protection against hyperoxia was directly related to the level of vitamin E supplementation. Selenium supplemented at 100 ppb provided significant protection when compared to 0 ppb or 1000 ppb. The latter dose may have been marginally toxic. We conclude that dietary supplementation of vitamin E and selenium may influence the relative susceptibility of an animal to pulmonary oxygen poisoning.
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PMID:Effect of dietary vitamin E or selenium on prostaglandin dehydrogenase in hyperoxic rat lung. 608 85

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

Weanling male rats were fed a semi-purified diet containing 10, 20, 40 or 60% of calories as fat having a constant polyunsaturated/saturated fatty acid ratio of 0.7. After 21-28 d of feeding, animals from each treatment group were exposed to pure oxygen at one atmosphere absolute for up to 72 h. Some animals were sacrificed after 0 or 48 h of oxygen exposure and lung tissue analyzed for the activities of the hexose monophosphate shunt and prostaglandin dehydrogenase/reductase. Other animals were exposed to hyperoxia until death. With increasing dietary fat content, the pre-exposure activities of the two enzymes decreased and oxygen-induced mortality increased. There was no dietary effect on enzyme activities after 48 h of hyperoxia. We concluded that both dietary fat content and the pre-exposure activity of prostaglandin dehydrogenase/reductase influenced the relative susceptibility to pulmonary oxygen poisoning.
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PMID:Effect of dietary fat on pulmonary enzymes and toxicity during normobaric hyperoxia. 711 50

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