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

Brief hypoxia or hyperoxia has been shown to affect growth and metabolism of chick embryos during the late stages of development. The objective of this study was to alter the availability of oxygen to chick embryos developing in ovo and to determine the effects on tissue zinc, copper, iron and manganese levels. On day 15 of incubation fertile chicken eggs were divided into three groups: 15% O2 (hypoxic), 60% O2 (hyperoxic) and 21% O2 (normoxic) and incubated under these conditions for 72 h to day 18. Hypoxia reduced embryo, heart, brain and liver wet weights, whereas hyperoxia increased embryo, heart, lung and liver wet weights compared to normoxic controls. Chorioallantoic membrane (CAM) wet weight was increased by hypoxia and reduced by hyperoxia. Livers from hyperoxic embryos contained more zinc, iron and manganese and less copper than livers from hypoxic or normoxic embryos. Tissue concentrations of zinc, copper, iron and manganese were reduced in brains from hyperoxic compared to hypoxic or normoxic embryos. Hyperoxia increased the zinc and copper concentrations in CAM, whereas hypoxia reduced zinc and iron levels. The contents of zinc and copper were increased in hyperoxic compared to normoxic or hypoxic lungs. Hearts from hyperoxic embryos had more zinc, copper and manganese than hypoxic or normoxic hearts. Hypoxic yolk sac contained more zinc and manganese than hyperoxic or normoxic yolk sac. Except for yolk sac, the trace element content of tissues from normoxic embryos increased from day 15 to day 18 of incubation in concert with tissue growth. We conclude that the availability of oxygen to the developing chick embryo affects tissue trace element levels through its effects on tissue growth, as a result of adaptation by specific tissues to different oxygen tensions, or via effects on the regulation of trace element uptake and assimilation by the tissues.
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PMID:Effects of brief hypoxia and hyperoxia on tissue trace element levels in the developing chick embryo. 166 14

This study reports the effects of valproic acid (VA) on the CD-1 mouse fetus when the drug is administered continuously via osmotic minipumps at human therapeutic drug plasma levels. Two VA-filled Alzet osmotic minipumps were implanted subcutaneously on gestation day 5 for continuous exposure of a total daily dosage of 850 mg/kg on gestation days 5-12. Dams were then exposed continuously to either normoxic (21% oxygen), hyperoxic (50% oxygen), or hypoxic (12% oxygen) controlled environments during gestation days 5-12, in order to determine if hyperoxic maternal conditions offered a protective environment for the fetus, and conversely, if hypoxia exacerbated teratogenicity. Dams were sacrificed on gestation day 18, and litter and fetal data were collected. It was determined in separate groups under normoxic conditions that the osmotic minipump system maintained VA plasma levels corresponding to human therapeutic levels. Sodium valproate was found to induce developmental toxicity in the CD-1 mouse fetus at human therapeutic drug plasma levels. Fetal weights were reduced, and the number of resorptions, deaths, and hematomas was increased. While hypoxia exacerbated the toxic effect on the fetus, hyperoxia failed to ameliorate the outcome.
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PMID:Effects of sodium valproate and oxygen on the CD-1 mouse fetus. 314 86

Oxidative stress may precondition the heart. The present study investigated whether hyperoxia elicits a preconditioning-like response. Rats were kept in a hyperoxic (>95% O2) environment for 60 or 180 minutes. Hearts were Langendorff-perfused immediately or 24 hours after hyperoxia, and exposed to 25 minutes of global ischemia and 60 minutes of reperfusion. Whole blood was sampled after 60 and 180 minutes of hyperoxia for oxidative stress markers. Hearts were sampled immediately or 24 hours after hyperoxia for measurement of antioxidants, lipid peroxidation products, heat shock protein 72 and endothelial nitric oxide synthase. At the end of reperfusion after 1 h hyperoxia, infarct size was determined by tetrazolium staining. Hyperoxia increased serum levels of conjugated dienes, reduced serum antioxidative protection, reduced reperfusion arrhythmias in most groups, and improved myocardial function. Infarct size was reduced from 45% of myocardial tissue in controls to 22% in treated animals. The myocardial activity of antioxidant enzymes, content of heat shock protein 72, and endothelial nitric oxide synthase in myocardial tissue were not influenced. In conclusion, hyperoxia induces a low-graded systemic oxidative stress, improves postischemic cardiac function and reduces infarct size. The mediators of protection remain to be determined.
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PMID:Pretreating rats with hyperoxia attenuates ischemia-reperfusion injury of the heart. 1126 75

Chronic hypoxia (CH) is believed to induce myocardial protection, but this is in contrast with clinical evidence. Here, we test the hypothesis that repeated brief reoxygenation episodes during prolonged CH improve myocardial tolerance to hypoxia-induced dysfunction. Male 5-week-old Sprague-Dawley rats (n = 7-9/group) were exposed for 2 weeks to CH (F(I)O(2) = 0.10), intermittent hypoxia (IH, same as CH, but 1 hr/day exposure to room air), or normoxia (N, F(I)O(2) = 0.21). Hearts were isolated, Langendorff perfused for 30 min with hypoxic medium (Krebs-Henseleit, PO(2) = 67 mmHg), and exposed to hyperoxia (PO(2) = 670 mm Hg). CH hearts displayed higher end-diastolic pressure, lower rate x pressure product, and higher vascular resistance than IH. During hypoxic perfusion, anaerobic mechanisms recruitment was similar in CH and IH hearts, but less than in N. Thus, despite differing only for 1 hr daily exposure to room air, CH and IH induced different responses in animal homeostasis, markers of oxidative stress, and myocardial tolerance to reoxygenation. We conclude that the protection in animals exposed to CH appears conferred by the hypoxic preconditioning due to the reoxygenation rather than by hypoxia per se.
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PMID:Chronic and intermittent hypoxia induce different degrees of myocardial tolerance to hypoxia-induced dysfunction. 1203 28