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

To study the ultrastructural effects of hyperoxia on the kidney, young adult Sprague Dawley rats were exposed to 3 atmospheres absolute (ATAs) of pure oxygen for 5 hours and were killed in a time sequence varying from immediately to 30 days after exposure. Their renal cortices were processed for electron microscopy. Selective mitochondrial changes were observed within sublethally and transiently altered proximal tubular epithelial cells. The most consistent finding was the accumulation of 0.08 mu to 0.5 mu round to ovoid homogeneous matrical inclusions which frequently formed larger confluent amorphous masses. The inclusions stained intensely with lead and uranium but appeared homogeneously electron-lucent in unstained sections. Energy-dispersive x-ray analysis revealed that they did not contain calcium or phosphorus. The inclusions were different from the innately electron-opaque flocculent densities commonly found in pathologically altered mitochondria. Since the mitochondria containing them were removed by autophagocytosis, it is suggested that the inclusions were associated with selective mitochondrial degeneration induced by hyperoxia. No glomerular lesions were found.
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PMID:Selective mitochondrial degeneration in renal tubules following hyperbaric oxygen exposure. 22 8

In anaesthetized cats, in which the cerebrospinal fluid bicarbonate concentration was varied by a ventriculocisternal perfusion technique, the ventilatory response to CO2 during hyperoxia could be satisfactorily described by VE = S(PCSFCO2 -B). Both the slope S and the intercept B were positively and linearly related to the CSF bicarbonate concentration. Assuming that the PCSFCO2 is equal to the PCO2 in extracellular fluid, it can be shown that VE is a linear, but not a unique function of the [H+] at the site of the chemoreceptors; the slope of this relation varies with the bicarbonate concentration at that site, possibly due to chemical complex formation between HCO-3 and Ca2+ or Mg2+. Changes in the B-value were related to the location of the central chemoreceptors with the models of Pappenheimer and Berndt aand their coworkers. It was found that changes in the CSF bicarbonate concentration are reflected for 60 per cent at the site of the central chemoreceptors, and that this was independent of the cerebral perfusion. Using Berndt's model a distance between CSF and central chemoreceptors of approximately 100 micron was found; this calculated distance is relatively insensitive to relationship (logarithmic or not) between ventilation and H+ concentration and to changes in cerebral perfusion, owing to the approximate nature of the diffusion model.
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PMID:Influence of the CSF bicarbonate concentration on the ventilatory response to CO2 in relation to the location of the central chemoreceptors. 74 Nov 4

The active and passive transport of radioactive calcium was studied in experiments on the brain and liver mitochondria, homogenates of brain and erythrocytes of albino rats subjected to the toxic effect of oxygen under pressure. The processes of the Ca2+ active transport preparations under examination are established to be inhibited after the effect of hyperoxia. The passive transport is considerably less dependent on the previous effect of oxygen. A conclusion is drawn on the prevailing sensitivity of the calcium energy-dependent transport to the damaging effect of hyperoxia.
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PMID:[Effect of hyperoxia on calcium transport in mitochondria of brain and liver]. 121 52

To determine whether platelet activating factor (PAF) plays a role in the responses seen in the fetal and transitional circulations, we assessed endogenous release of PAF in cultured fetal ovine endothelial cells from the pulmonary artery (PA), ductus arteriosus (DA) and aorta (Ao) under basal conditions and following exposure to hypoxia or hyperoxia. The cells were prelabeled with [3H] acetate and subsequently exposed to different ambient oxygen concentrations, i.e., 95% O2 or 95% N2, balance CO2, using calcium ionophore as a positive control. The effect of indomethacin on DA endothelial PAF production following stimulation with ionophore was also established. Synthesis of [3H] PAF was measured by counts comigrating on TLC with unlabeled PAF. We found that PAF production by fetal ovine PA, Ao and DA cells was similar and unaffected by hypoxia or hyperoxia. Exposure of ionophore stimulated DA cells to indomethacin was, however, associated with a decrease in PAF production (p less than 0.05). We speculate that in vitro alterations in ambient O2 concentration do not influence fetal ovine endothelial PAF production but indomethacin may decrease PAF production in the DA.
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PMID:Effect of ambient oxygen changes on platelet activating factor production by fetal ovine endothelial cells. 186 26

Microscopic fluorometry was used to examine the effects of anoxia and cyanide (CN-) on cytosolic calcium [Ca2+]i of cultured carotid body (CB) glomus cells from newborn rabbits. Applications of high K+ and veratridine (VRT), a sodium channel activator, induced rapid and marked increases in [Ca2+]i. These effects were inhibited by D600 a calcium channel blocker. [Ca2+]i changes induced by VRT were also blocked by tetrodotoxin (TTX). Glomus cells exhibited a slow increase in [Ca2+]i in response to anoxia and CN-, and a slight decrease during hyperoxia. The effects of anoxia and CN- were blocked by D600 but not by TTX. We conclude that these stimuli induce calcium entry into glomus cells via voltage-dependent Ca2+ channels. Voltage-dependent Na+ channels were not involved.
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PMID:Response of cytosolic calcium to anoxia and cyanide in cultured glomus cells of newborn rabbit carotid body. 191 62

A study was made of the blood and tissue oxygen regime in patients with vibratory disease (VD) induced by local vibration and of the importance of lipid peroxidation (LPO) in oxygenation disorders. Venous hyperoxia, a decrease of the arteriovenous difference according to oxygen, the percentage of oxygen utilization by tissues, shift of the acid-base balance towards metabolic acidosis were established, attesting to tissue hypoxia that increased with the gravity of VD. The importance of a steady activation of LPO and depression of the antioxidant system in the pathogenesis of hypoxia associated with VD was supported by the correlation analysis data on oxygen balance and LPO, the functional and metabolic characteristics of red blood cells (according to the viscosity of red blood cell suspension and the content in the cells of SH-groups, lipoproteins and histidine) and platelets (according to aggregation in response to ADP and thrombin) as well as by the level of blood serum fluorescence. The authors provide evidence for the use of antioxidants (a complex of alpha-tocopherol with ascorbic acid and methionine and calcium antagonists of the nifedipine group), giving a membranostabilizing effect, in multimodality treatment of patients afflicted with VD.
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PMID:[Cell-membrane aspects of the pathogenesis of hypoxia in vibration disease induced by local vibration]. 204 32

Metabolites of arachidonic acid (AA) released into bronchoalveolar lavage fluid of animals exposed to hyperoxia have previously been implicated as mediators of pulmonary oxygen toxicity. The alveolar macrophage (AM) represents an important potential source of these eicosanoids. We have therefore investigated the effects of in vitro hyperoxia (95% O2/5% CO2) versus normoxia (95% air/5% CO2) on the metabolism of AA in the AM of the rat. Exposure to 95% O2 for up to 72 h did not impair the viability or affect the protein content of cultured AMs. Hyperoxia for 24 to 72 h increased the accumulation of free AA liberated from endogenous stores in cultures of resting AMs. Despite this increase in free AA, no changes in synthesis of thromboxane B2, prostaglandin (PG) E2, PGF2 alpha, leukotriene (LT) B4, or LTC4 were observed in resting AMs exposed to hyperoxia for up to 72 h. This was not due to degradation of eicosanoids in hyperoxia. However, formation of cyclooxygenase metabolites from exogenously supplied AA was reduced in hyperoxia-incubated AMs, suggesting that hyperoxia inhibited the cyclooxygenase enzyme. In AMs stimulated with calcium ionophore A23187, both AA release and synthesis of cyclooxygenase and lipoxygenase eicosanoids were augmented after incubation in hyperoxia for 24 to 72 h. The increase in A23187-stimulated LTB4 synthesis caused by hyperoxia was inhibited by the antioxidants catalase, superoxide dismutase, and the intracellular cysteine loading agent L-2-oxothiazolidine-4-carboxylic acid, suggesting that the augmentation by hyperoxia of A23187-induced AA metabolism was mediated by reactive oxygen metabolites. Thus, hyperoxia has complex effects on AA metabolism in the AM, which include the ability to augment the release of AA and formation of bioactive eicosanoids. These findings support a possible role for eicosanoid synthesis by the AM in the pathogenesis of oxygen toxicity of the lung.
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PMID:Complex effects of in vitro hyperoxia on alveolar macrophage arachidonic acid metabolism. 215 14

We compared oxygen-related prostaglandin synthesis in fetal lamb ductus arteriosus (DA) pulmonary artery (PA) and aorta endothelial and smooth muscle cells. We measured basal synthesis of 6-keto-PGF1 alpha and PGE2, the response to calcium ionophore (A23187), a nonspecific stimulus of prostaglandin production, as well as the response to oxygen, a perinatal stimulus, monitoring both the effects of hyperoxia (95% O2) and hypoxia (2% O2). In addition, we established whether differences observed in fetal lamb PA cells related to oxygen tension were also observed in newborn central and microvessel PA cells. Our results indicate that DA endothelial cells increase 6-keto-PGF1 alpha in response to ionophore (p less than 0.05). With hyperoxia, DA endothelial cells increase PGE2 synthesis and DA smooth muscle cells increase 6-keto-PGF1 alpha (p less than 0.05 and 0.02, respectively). Aorta smooth muscle cells increase 6-keto-PGF1 alpha in response to ionophore and hyperoxia (p less than 0.003 and 0.05, respectively). PA endothelial and smooth muscle cells have higher levels of basal prostaglandin synthesis when compared with DA and aorta. In response to ionophore, increased 6-keto-PGF1 alpha is observed in both PA endothelial and smooth muscle cells (p less than 0.02 and 0.0004, respectively), and PGE2 is increased in PA smooth muscle cells (p less than 0.003). Hypoxia, however, decreases PA smooth muscle production of both 6-keto-PGF1 alpha and PGE2 (p less than 0.02 and 0.01, respectively). Similar observations were made in newborn lamb central and microvessel PA cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxygen-related prostaglandin synthesis in ductus arteriosus and other vascular cells. 250 51

1. Noradrenaline (NA;ED90) caused a contraction of the rat aorta which could be separated into two components, a rapid response mediated by release of intracellular Ca2+ and a more slowly developing contraction which relied principally upon Ca2+ influx. 2. Exposure to acute (30 min) hypoxia has been previously shown to reduce the NA-induced contraction (by 28.0 +/- 2.7%, n = 168) which recovered completely upon re-oxygenation (recovery response). In the present study, prolonged exposure to hypoxia (70 h) caused a more pronounced reduction (39.7 +/- 3.0%, n = 90) of the NA-induced contraction, but, re-oxygenation then produced incomplete recovery to 77.9 +/- 3.9% (n = 90) of the control response. 3. Prolonged exposure to 95% O2 caused a 36.5 +/- 3.1% (n = 42) reduction of NA-induced contractions, whereas prolonged exposure to 21% O2 only caused a small (12.6 +/- 3.4%, n = 6) depression of these responses. 4. The component of the NA-induced contraction mediated by release of intracellular Ca2+ is 39.8 +/- 1.3% (n = 83) of the NA contraction in Ca-containing Krebs solution and was previously found to be unaffected by acute hypoxia. However, following prolonged exposure to either hypoxia or 21% O2, this component only reached 30.7 +/- 2.2% (n = 32) or 28.3 +/- 0.9% (n = 6) of the control response, respectively. Prolonged exposure to 95% O2 caused a more pronounced reduction of this component of contraction which then reached 19.1 +/- 2.1% (n = 12) of the control response. 5. Verapamil (10nM-10 microM) produced similar concentration-dependent reductions of NA-induced contractions elicited during control conditions or acute hypoxia; under these conditions, 1 microM verapamil caused a 34.1 + 6.9% (n = 6) and a 41.8 + 2.9% (n = 18) reduction of these responses respectively. However, recovery responses caused by re-oxygenation of tissues exposed to acute hypoxia were more sensitive to verapamil which, at a concentration of 1 microM, caused a 59.2 + 2.7% (n = 18) reduction of these responses. Verapamil (10 nM-10 microM) also caused similar pronounced concentration-dependent reductions of contractions elicited during prolonged exposure to normoxia or hyperoxia and of recovery responses obtained following re-oxygenation of tissues exposed to prolonged hypoxia; 1 microM verapamil caused a 62.5 + 1.1% (n = 6), 77.2 + 3.8% (n = 12) and a 68.0 + 4.3% (n = 12) reduction of these responses respectively. In contrast, contractions elicited during prolonged hypoxia were less sensitive to verapamil which at a concentration of 1 microM only caused a 16.2 + 2.2% (n 12) reduction of these responses. 6. The present study indicates that prolonged exposure of the rat aorta to either hypoxic or oxygenated conditions causes attenuation of NA-induced contraction. However, these effects are also accompanied by changes in tissue Ca2+ handling which differ under each condition and might account for the observed modifications in tissue sensitivity to the calcium-entry blocker verapamil.
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PMID:The effects of verapamil upon noradrenaline-induced contraction of the rat isolated aorta following acute and prolonged alterations in PO2. 261 85

Iron administration results in the development of oxidative stress in skeletal muscles, as evidenced by increases in amounts of lipid oxidation fluorescent end products, decreases in vitamin E concentration, and inhibition of calcium transport by sarcoplasmic reticulum. Exhaustive physical loading or hyperoxia, or their combination, does not lead to apparent modification in calcium transport by sarcoplasmic reticulum in skeletal muscle homogenates. However, physical loading or hyperoxia does in fact induce oxidative stress since they magnify the effect of iron loading on the inhibition of calcium transport.
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PMID:Oxidative stress leads to inhibition of calcium transport by sarcoplasmic reticulum in skeletal muscle. 292 49


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