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)

Salt-soluble proteins of great hemispheres of rats, intact and those subjected to the effect of hyperbarooxigenation, were separated by DEAE-cellulose chromatography into 10 heterogenous fractions, each of them containing 5-12 subfractions. The content of glucosamine and sialic acid was determined in each of the isolated fractions. Changes in the degree of heterogeneity and in total content of protein in the fractions as well as variations in the content of carbohydrate components in the chromatographic fractions are observed under the effect of hyperoxia.
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PMID:[Nervous tissue glycoproteins normally and under the action of oxygen under pressure]. 94 8

Bacterial endotoxin has a marked protective effect against pulmonary O2 toxicity in rats placed directly in atmospheres of greater than 95% O2. To determine whether endotoxin treatment during exposure to relatively low levels of hyperoxia would protect rats from the accelerated O2 toxicity that normally occurs when these rats are transferred to greater than 95% O2, we gave endotoxin or saline 1) during exposure to 40% O2 (5 days), or 2) during exposure to 40%-60%-85% O2 (2 days at each level). Saline-treated rats showed significantly decreased tolerance on transfer to greater than 95% O2 [LT50 = 47.5 h (exposure 1) and 48.5 h (exposure 2)] compared with normal nonpreexposed rats (LT50 = 66 h). In contrast, endotoxin-treated rats showed a marked tolerance on transfer to greater than 95% O2 [% of rats surviving 72 h = 14/16 (88%) endotoxin-treated vs. 2/16 (13%) saline-treated]. The endotoxin-treated rats, unlike the saline-treated rats, showed significant elevations in lung superoxide dismutase, catalase, glutathione peroxidase, and glucose-6-phosphate dehydrogenase levels after the O2 preexposure periods; this may account for their significantly improved tolerance when challenged with greater than 95% O2 exposure.
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PMID:Endotoxin reverses the decreased tolerance of rats to greater than 95% O2 after preexposure to lower O2. 732 58

To assess the roles of cyclooxygenase inhibition and hyperoxia in regulating pulmonary perfusion, we studied 13 dogs with diffuse granulomatous lung disease (DGLD) and 13 normal dogs. Baseline observations were obtained at fractional inspired O2 (FIO2) 0.21 and 1.0 and repeated after infusion of meclofenamate (Mec; n = 8) or saline (n = 5). Resistance to flow was evaluated from the pulmonary end-diastolic gradient (PDG) and by ohmic pulmonary vascular resistance (PVR). Distribution of blood flow was evaluated with sulfur hexafluoride in DGLD and with multiple inert gas alveolar ventilation-perfusion (VA/Q) plots in normal dogs. Before infusion, there were no differences between the saline and Mec groups at either FIO2. Saline induced no significant changes at either FIO2. After Mec in DGLD, PDG at FIO2 0.21 rose from 4 +/- 2 to 6 +/- 4 mmHg (P < 0.04), PVR increased from 297 +/- 98 to 484 +/- 181 dyn.s.cm-5.m-2 (P < 0.01), whereas shunt flow (Qs/Qt) fell form 13.6 +/- 12.0 to 6.2 +/- 5.3% (P < 0.03). At FIO2 1.0 PDG rose from 3 +/- 2 to 4 +/- 3 mmHg (P < 0.02), PVR increased from 262 +/- 78 to 374 +/- 139 dyn.s.cm-5.m-2 (P < 0.01), whereas Qs/Qt fell from 14.5 +/- 13.3 to 6.4 +/- 5.2% (P < 0.02). After Mec in normal dogs, PDG at FIO2 0.21 rose from 3 +/- 1 to 4 +/- 1 mmHg (P < 0.015) and PVR increased from 256 +/- 92 to 340 +/- 101 dyn.s.cm-5.m-2 (P < 0.05); at FIO2 1.0 PDG and PVR were unchanged from preinfusion levels. In normal dogs, no parameters of VA/Q changed significantly with hyperoxia or Mec. These data suggest that perivascular inflammation enhances perfusion in DGLD by elaboration of vasodilator prostaglandins (PG). By inhibiting PG synthesis, Mec selectively increases resistance in diseased lung at FIO2 0.21 and lowers Qs/Qt. In contrast, there was vasoconstriction without flow redistribution in normal dogs, suggesting that vasodilator PGs contribute to the low tone in the normal pulmonary bed. The vasodilation without flow redistribution in both models during hyperoxia after Mec suggests an effect of O2 that is related neither to PG synthesis nor to hypoxic vasoconstriction.
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PMID:Role of cyclooxygenase inhibition and hyperoxia in regulating pulmonary perfusion in dogs. 773 53

Rabbit corneas were incubated, over 4 h in vitro, with the corneal epithelial surface exposed to various solutions to assess their utility as incubation solutions for physiological, pharmaceutical or toxicological studies. The corneal endothelium was perfused with a 35 mM bicarbonate-mixed salts solution equilibrated at 36 degrees C. Corneal thickness, corneal hydration or epithelial cell appearance (as assessed by scanning electron microscopy) were found to be similar to in vivo if a 35 mM bicarbonate, mixed salts solution (equilibrated with 5% CO2-air) was used for the epithelium. Some swelling (14 microns h-1), increased hydration and minor cell exfoliation were seen if this 35 mM bicarbonate solution was equilibrated with 5% CO2-95% O2 (hyperoxia). Solutions with only 5 mM bicarbonate (0.5% CO2-air) produced rapid swelling, large increases in hydration and marked cellular damage. Slightly hypertonic (310 mOsm kg-1) solutions containing 5 mM bicarbonate caused some swelling at 15 microns h-1, small increases in hydration and some cell damage but the swelling and cellular damage were further reduced by making the solution slightly more hypertonic (325 mOsm kg-1) by addition of NaCl and KCl. Saline (NaCl 0.9% or 0.97%) or phosphate-buffered saline (PBS) (300 mOsm kg-1) produced swelling at 21-28 microns h-1, 30% increases in hydration and almost total destruction of the superficial cell layers. These studies confirm in vivo experiments that saline (and also buffered saline solutions) are rather toxic to the corneal epithelium and thus should not be used as epithelial incubation solutions. Even when using mixed salts solutions and even with bicarbonate present, small differences in composition can have marked effects on corneal thickness, hydration or cell appearance. Hyperoxic solutions appear to be mildly cytotoxic compared with normoxic solutions.
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PMID:Evaluation of the effects of saline versus bicarbonate-containing mixed salts solutions on rabbit corneal epithelium in vitro. 859 30

Fast scan cyclic voltammetry (FSV) with a nanostructured carbon fiber sensor (N-CFS) was developed for direct measurements of the purine metabolite 2,8-dihydroxyadenine (2,8-DHA; i.e. 6-amino-1H-purine-2,8-dione) in endothelial cell supernatants as a marker of cell stress. The 2,8-DHA was measured in the supernatant of aortic (AECs) and pulmonary artery endothelial cells (PAECs), which were maintained in Hank's Balanced Salt solution (HBSS) and exposed to physiological oxygen pressures as well as to oxidative stress, hypoxia (specifically 3% O(2) for AECs) and hyperoxia (20% O(2) for PAECs). Dilution of the supernatants with phosphate buffer in the ratio of 1 : 5 allowed the optimization of FSV measurements with the N-CFS in cell supernatants.The LOD for 2,8-DHA was 1 microM and the LDR was 2-15 microM with the sensitivity of (0.34 +/- 0.01) nA microM(-1) (R(2) = 0.99). The changes in 2,8-DHA concentration when the cells were exposed to stress confirm that PAECs can adapt to stress. However, the results also show that the tolerance of AECs to hypoxia is low. Cellular pathways involved in the response of PAECs and AECs to oxidative stress are outlined.
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PMID:Rapid measurements of 2,8-dihydroxyadenine (2,8-DHA) with a nanostructured electrochemical sensor in 5-fold diluted supernatants of endothelial cells exposed to oxidative stress. 2009 61

Cisplatin (CP) nephrotoxicity is mainly due to reactive oxygen species. Oxygen pre-exposure as a mild oxidative stress may enhance some endogenous defense mechanisms, so its effect on cisplatin-induced acute renal failure was investigated in present study. Twenty-four rats were divided into four groups. The O(2)+ CP and Air + CP groups were were subjected to i.p. injection of 5 mg/kg cisplatin, and in the Air + Saline and O(2) + Saline groups, saline was injected instead of cisplatin. O(2)+ CP and O(2)+ Saline groups were pretreated with oxygen (3h/d for two days), and the other two groups were pretreated with room air. Cisplatin was administered 24 h after last pretreatment session. Three days after cisplatin injection, plasma samples were obtained, and parts of kidney tissue were frozen for biochemical analysis or fixed in formalin for histological assessments. Preconditioning with oxygen prior to cisplatin administration led to reduced tubular necrosis and luminal cast formation and improvement of renal function, as was evidenced by significant reduction in plasma creatinine and urea levels. Oxygen pretreatment also significantly reversed cisplatin-induced reduction in renal catalase activity and glutathione level. It could be concluded that oxygen pretreatment could have a delayed protective effect against cisplatin nephrotoxicity, and that increased renal catalase activity may be involved in this protective effect of hyperoxia.
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PMID:Pretreatment with oxygen protects rat kidney from cisplatin nephrotoxicity. 2019 86

This laboratory previously reported that zymosan priming protects rats against pulmonary oxygen toxicity. That study used a standard priming protocol (3 daily intravenous injections [15 mg zymosan/rat] with 2 days' rest) before hyperoxia. This study confirms that report and more fully characterizes the zymosan priming model. Three studies were conducted to establish the (1) effects of dosage, (2) role of duration of rest period between injections and hyperoxia and (3) importance of injection number, on protection by zymosan priming. Rats were exposed to >95% oxygen for 52 h or room air and acute lung injury was quantitated using standard methods. Lung injury decreased (P < 0.05 versus saline controls) in all groups of zymosan-primed rats (3 daily intravenous injections [1-15 mg zymosan/rat] with 2 days' rest before hyperoxia). Although the differences between zymosan-primed groups were not statistically significant, protection (as indicated by decreasing mean values of measured parameters of lung injury) increased with dosage. A one-day rest after injections was sufficient to partially protect zymosan-primed rats from hyperoxia (some measured parameters in the zymosan-primed group differed significantly from comparable values in the Saline group), but full protection (all measured parameters within a group differed significantly from Saline values) was not produced until rats received two days' rest before hyperoxia. Finally, one or two zymosan treatments produced partial protection against oxygen toxicity but three injections were needed to produce full protection. In conclusion, this study found that the standard priming protocol (3 zymosan injections with 2 days' rest before hyperoxia) was the most effective in protecting rats against hyperoxia.
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PMID:Zymosan priming protects rats against pulmonary oxygen toxicity: characterization of the model. 2040 31