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

An investigation of acid and neutral triacylglycerol lipases in rat lung tissue has been carried out. The effect of high oxygen concentration in the inspired gas mixture on the activities of the two triacylglycerol lipases has been studied. Hyperoxia had a strong inhibitory effect on both enzymes, the degree of inhibition being dependent on the duration of exposure. Dibutyryl-3',5' AMP and NaF restored completely the activities of the inhibited triacylglycerol lipases, while adrenaline and caffeine had no effect. The possible mechanisms of the effects of oxygen on lung triacylglycerol lipases are discussed.
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PMID:[Effect of hyperoxia on triacylglycerol lipase activity of the rat lung (author's transl)]. 19 50

Erythropoietin (Ep) levels in spent culture media of a Hep G2 human hepatoblastoma cell line were measured by radioimmunoassay (RIA), fetal mouse liver erythroid colony formation (FMLC), and the exhypoxic polycythemic mouse assay (EHPCMA). The Hep G2 cells at high density produced approximately 700 mU/ml Ep when measured with the RIA. On the other hand, the Ep levels when assayed in EHPCMA and FMLC were 50 and 2,600 mU/ml, respectively. The bioactivity in FMLC was completely neutralized by an antibody to purified human recombinant Ep, indicating that the erythropoietic activity in the Hep G2 spent culture medium was immunologically equivalent to Ep. Ep levels in the medium from low-density Hep G2 cells in 5% O2 and 1% O2 were 2.5- and 4-fold greater, respectively, than that of 20% O2. In contrast, hyperoxia (40% O2) significantly inhibited Ep production. A significant increase in Ep secretion was also observed when the cells were incubated with cobaltous chloride (2 X 10(-6) -2.5 X 10(-4) M). Tunicamycin (0.5 micrograms/ml), which inhibits N-linked glycosylation, significantly reduced the enhancement of Ep secretion induced by hypoxia (1% O2) without affecting cell growth. Forskolin and cholera toxin, each of which increased the levels of cyclic AMP in the Hep G2 cells by 40-fold, produced a significant (P less than 0.05) further increase in Ep secretion in the presence of hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhanced erythropoietin secretion in hepatoblastoma cells in response to hypoxia. 255 19

The level of adenosine was measured in monthly biopsied livers from rats fed ethanol and a high fat/low protein diet in order to test a hypothesis that hepatic adenosine is increased due to enhanced breakdown of adenine nucleotides in which ATP and total adenylate pool were decreased by chronic ethanol feeding. The ethanol-fed rats showed a significantly higher average level of adenosine compared to the pair-fed controls. When investigated monthly, however, adenosine in ethanol-fed rats increased only after the decrease in ATP had stabilized and AMP remained unchanged, indicating that these changes were not temporarily related. The average percentage of change in adenosine after acute hyperoxia or hypoxia were variable both in ethanol-fed and pair-fed rats. There was a tendency for a positive correlation between the percentage of change of adenosine and AMP after hyperoxia regardless of ethanol feeding. A negative correlation between the percentage of change of adenosine and energy charge, and a positive correlation between the percentage of change of adenosine and AMP were seen after hypoxia regardless of ethanol feeding. Adenosine levels changed rapidly in response to changes in systemic of pO2 in both the ethanol-fed and control rats, indicating that the liver maintained its normal response to the changes in energy state. The results indicate that chronic ethanol feeding does increase the level of adenosine in the liver and that this level remains responsive to acute changes in pO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatic adenosine in rats fed ethanol: effect of acute hyperoxia or hypoxia. 305 72

For almost 10 years, numerous studies have shown that the pulmonary endothelium is endowed with a certain number of metabolic properties related to the uptake and hydrolysis of circulating vasoactive substances. Noradrenaline, serotonin, adenosine and possible certain prostaglandins are transported in the endothelial cells, according to processes which have now been clearly defined, and are there metabolised. Other compounds, including peptides (bradykinin, angiotensin I), or nucleotides (ATP, ADP, AMP) are hydrolysed in contact with the plasma membrane of the endothelium, without penetrating within the cell. For certain substrates (serotonin, angiotensin I), the properties of the pulmonary endothelial cell may be extended to systemic endothelial cells. For other substances, there would appear to be a specificity of endothelial function according to the site. It would appear that the lung, by virtue of its richness in endothelial cells, is capable of influencing concentrations of the circulating substances and, as a result, vascular tone. The existence of delicate processes of the uptake of substances has also been used to test the integrity of the cellular function of the pulmonary endothelium under experimental pathological condition, such as hyperoxia. However, before such a technique, based upon measurement os extraction of amines or other substances from various parts of the pulmonary circulation could be applied clinically, a critical consideration must be undertaken of the multiple factors involved in these processes. The major problem lies in the difficulty of distinguishing between dysfunction of the endothelial cells or a decrease in their number.
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PMID:[Measurement of pulmonary endothelial function; its potential clinical value]. 611 Dec 67

Treatment of newborns with 20 mg/kg/day chlorphentermine orally for 1 week increased incorporation of thymidine into lung DNA without an associated change in tissue morphology or cyclic AMP levels. An increase in chlorphentermine dose to 60 mg/kg resulted in an accumulation of alveolar hypertrophic macrophages and a rise in incorporation of thymidine into lung DNA; however, cyclic AMP levels were decreased. In contrast, 20 or 60 mg/kg/day for 1 week phentermine-induced depression in the incorporation of thymidine into pulmonary DNA was accompanied by a decrease in cyclic AMP but no apparent alteration in tissue morphology. Hyperoxia did not modify the phentermine-induced changes in cyclic AMP levels and pulmonary ultrastructure. In contrast, hyperoxia altered the responsiveness of newborns to 20 mg/kg chlorphentermine as evidenced by the presence of foam cells. Data suggest that the chlorphentermine-induced increase in DNA synthesis in newborn lung seems independent of changes in cyclic AMP and tha modification of drug-induced alterations by hyperoxia may be related to the chemical structure of a compound.
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PMID:Modification by hyperoxia of chlorphentermine- or phentermine- induced effects on newborn rat lung morphology and metabolism. 627 4

We analyzed brain tissue in 139 rats for adenosine and its metabolites, inosine and hypoxanthine, during the initial 120 seconds of seizures induced by bicuculline. We also measured ATP, ADP, AMP, phosphocreatine (PCr), and lactate. We divided the rats into four groups by adjustment of their preictal arterial oxygen tension: group I, PaO2 > 200 mm Hg; group II PaO2 = 50 mm Hg; and group III: PaO2 = 100 mm Hg. We treated a fourth group whose PaO2 = 100 mm Hg with phentolamine to block the 44% rise in blood pressure which occurred with the onset of seizures. PaCO2 was maintained between 30 anf 40 mm Hg in all groups. Brain tissue was sampled rapidly after 0, 10, 20, 30, 60, and 120 seconds of seizures by the freeze-blow technique. With normoxia (PaO2 = 100 mm Hg) or hyperoxia (PaO2 > 200 mm Hg), adenosine increased within ten seconds of the onset of seizures and remained elevated even after 120 seconds. Elevations in inosine and hypoxanthine were delayed compared to the increases in adenosine. A reduction in PaO2 (50 mm Hg) or systemic blood pressure during seizures caused a further augmentation in the increase in brain adenosine levels. During the seizure period, transient changes in adenine nucleotides and energy charge were observed, but PCr remained depressed and lactate continued to rise. The rapid and sustained increase in cerebral adenosine levels, temporally paralleling the changes in cerebral blood flow, supports the role for adenosine in the regulation of cerebral blood flow.
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PMID:Changes in brain adenosine during bicuculline-induced seizures in rats. Effects of hypoxia and altered systemic blood pressure. 677 98

Breathing of 100% oxygen at ambient pressure causes disorders in mouse brain organic phosphate phosphocreatine (PC), ATP, ADP, and AMP. The fast increase in PC level attains a maximum augmentation of about 50% after 16-18 h of exposure with subsequent slight alterations between 18 and 50 h. The initial losses (a) in ATP amount to approximately 20% after 4 h; (b) in ADP, 32% after 6-8 h; and (c) in AMP, about 40% after 30 min and 50% after 50 h. contrary to the continual decrease in AMP, the ATP and ADP values exhibit a later increase to a constant level during the full time of exposure up to 50 h. The initial loss in adenosine nucleotides points to an intense effect of hyperoxia in nerve cell metabolism with subsequent attainment of a new adenylate equilibrium at lower concentrations. The increased but constant level of PC may be due to an inhibition of the oxygen sensitive SH-groups, which are an essential center in the creatine kinase. Although the absolute concentration of AMP is by far the lowest of the three nucleotides, the continual decrease in AMP is of considerable importance because of its direct response to ATP via adenylate kinase reaction.
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PMID:Brain energy metabolism in mice exposed to oxygen at 1 atmosphere absolute. 733 82

Hypoxia is the alleged stimulus for initiation of increase of carbonic anhydrase II (CAII) and 2,3-diphosphoglycerate (2,3-DPG) synthesis of red blood cells from late chick embryos. The PO2-dependent regulation of red cell metabolism is mediated by unknown humoral factors [Million et al., Am. J. Physiol. 261 (Regulatory Integrative Comp. Physiol. 30): R1188-R1196, 1991]. In the present investigation we have analyzed whether interindividual differences in egg size (which result in different surface area-to-mass ratios) affect the timing of initiation of 2,3-DPG and CAII synthesis in late chick embryos. We also investigated the effect of extracellular adenine nucleotides on red cell organic phosphate pattern and O2 affinity to test whether the inhibitory effect of normal or elevated PO2 on 2,3-DPG synthesis and the concomitant increase of ATP (and O2 half-saturation pressure) can be mimicked by these agents. The results show that differences in egg size affect the timing of CAII and 2,3-DPG synthesis, indicating that PO2-dependent regulation of red cell function allows adjustment to the properties of the individual egg. We also found that extracellular ATP, which is rapidly degraded to AMP by red cell ectoenzymes, can alter the red cell phosphate pattern and O2 affinity, i.e., significantly increase red cell ATP, decrease red cell 2,3-DPG and O2 affinity, and thus mimic the effect of normoxia and hyperoxia. These findings suggest that extracellular adenine nucleotides may be involved in the PO2-dependent regulation of embryonic red cell metabolism.
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PMID:Control of red cell function of late chick embryos: role of extracellular ATP/AMP and egg size. 806 66

We hypothesized that manganese superoxide dismutase (MnSOD), known to be induced in rat mesothelial cells by asbestos fibers, cytokines, and hyperoxia, may also be induced in asbestos-related pleural diseases such as mesothelioma. MnSOD was assessed in healthy human pleural mesothelium (n = 6), in biopsy samples of human pleural mesothelioma (n = 7), in transformed nonmalignant human mesothelial cells (Met5A), and in two human mesothelioma cell lines (M14K and M38K) established from the tumor tissue of mesothelioma patients. There was no MnSOD immunoreactivity in five of the six samples of healthy pleural mesothelium, whereas MnSOD immunoreactivity was high in the tumor cells in all the mesothelioma samples. Northern blotting, immunohistochemistry, Western blotting, and specific activity measurements showed lower MnSOD in the nonmalignant Met5A mesothelial cells than in the M14K and M38K mesothelioma cells. In additional experiments the mesothelial and mesothelioma cells were exposed to menadione, which generates superoxide intracellularly, and to epirubicin, a cytotoxic drug commonly used to treat mesothelioma. The M38K mesothelioma cells were most resistant to menadione and epirubicin when assessed by LDH release or by adenine nucleotide (ATP, ADP, and AMP) depletion. These same cells showed not only the highest MnSOD levels, but also the highest mRNA levels and activities of catalase, whereas glutathione peroxidase and glutathione reductase levels did not differ significantly. We conclude that MnSOD expression is low in healthy human pleural mesothelium and high in human malignant mesothelioma. The most resistant mesothelioma cells contained coordinated induction of MnSOD and catalase.
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PMID:Manganese superoxide dismutase in healthy human pleural mesothelium and in malignant pleural mesothelioma. 953 46

The carotid body is a peripheral sensory organ that can transduce modest falls in the arterial PO(2) (partial pressure of oxygen) into a neural signal that provides the afferent limb of a set of stereotypic cardiorespiratory reflexes that are graded according to the intensity of the stimulus. The stimulus sensed is tissue PO(2) and this can be estimated to be around 50 mmHg during arterial normoxia, falling to between 10-40 mmHg during hypoxia. The chemoafferent hypoxia stimulus-response curve is exponential, rising in discharge frequency with falling PO(2), and with no absolute threshold apparent in hyperoxia. Although the oxygen sensor has not been definitely identified, it is believed to reside within type I cells of the carotid body, and presently two major hypotheses have been put forward to account for the sensing mechanism. The first relies upon alterations in the cell energy status that is sensed by the cytosolic enzyme AMPK (AMP-activated protein kinase) subsequent to hypoxia-induced increases in the cellular AMP/ATP ratio during hypoxia. AMPK is localized close to the plasma membrane and its activation can inhibit both large conductance, calcium-activated potassium (BK) and background, TASK-like potassium channels, inducing membrane depolarization, voltage-gated calcium entry and neurosecretion of a range of transmitter and modulator substances, including catecholamines, ATP and acetylcholine. The alternative hypothesis considers a role for haemoxygenase-2, which uses oxygen as a substrate and may act to gate an associated BK channel through the action of its products, carbon monoxide and possibly haem. It is likely however, that these and other hypotheses of oxygen transduction are not mutually exclusive and that each plays a role, via its own particular sensitivity, in shaping the full response of this organ between hyperoxia and anoxia.
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PMID:Sensing hypoxia in the carotid body: from stimulus to response. 1770 92


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