UMLS:C0242706 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Target Concepts:

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

Exposure of cells to oxygen concentrations higher than normal (hyperoxia) damages the molecular components of cells, resulting in cellular dysfunction and death. Metformin, a biguanide molecule used for treating non-insulin-dependent diabetes, been shown to lower blood pressure. The aim of this study was to investigate the possible effects of hyperoxia and metformin on the vascular responses of thoracic aorta to vasoactive compounds, using an in vitro rat model. In the hyperoxia-control (HC) group, the response to acetylcholine was completely abolished, but metformin treatment before (MH) or after (HM) exposure to 100% oxygen restored the response to acetylcholine to near-control values. In aortas from HC, MH, or HM groups, no significant differences were found in pD2 values to the endothelium-dependent vasodilator sodium nitroprussiate. In aortic strips from metformin-treated rats, the pD2 values for noradrenaline in the presence of endothelium were significantly smaller than those in the normal control group. The maximal contractile responses to KCl were not significantly different among all experimental groups. The results of the present study show that in hyperoxia-exposed rats, metformin treatment reverses the abolished vascular relaxation to AChe.
...
PMID:Effect of hyperoxia and metformin on vascular responses to vasoactive compounds in rats. 1176 94

Changes in branchial vacuolar-type H(+)-ATPase B-subunit mRNA and Na+, K(+)-ATPase alpha- and beta-subunit mRNA and ATP hydrolytic activity were examined in smolting Atlantic salmon exposed to hyperoxic and/or hypercapnic fresh water. Pre-smolts, smolts, and post-smolts were exposed for 1 to 4 days to hyperoxia (100% O2) and/or hypercapnia (2% CO2). Exposure to hypercapnic water for 4 days consistently decreased gill vacuolar-type H(+)-ATPase B-subunit mRNA levels. Salmon exposed to hyperoxia had either decreased or unchanged levels of gill B-subunit mRNA. Combined hyperoxia + hypercapnia decreased B-subunit mRNA levels, although not to the same degree as hypercapnic treatment alone. Hyperoxia generally increased Na+, K(+)-ATPase alpha- and beta-subunit mRNA levels, whereas hypercapnia reduced mRNA levels in presmolts (beta) and smolts (alpha and beta). Despite these changes in mRNA levels, whole tissue Na+, K(+)-ATPase activity was generally unaffected by the experimental treatments. We suggest that the reduced expression of branchial vacuolar-type H(+)-ATPase B-subunit mRNA observed during internal hypercapnic acidosis may lead to reduction of functional V-type H(+)-ATPase abundance as a compensatory response in order to minimise intracellular HCO3- formation in epithelial cells.
...
PMID:Vacuolar-type H(+)-ATPase and Na+, K(+)-ATPase expression in gills of Atlantic salmon (Salmo salar) during isolated and combined exposure to hyperoxia and hypercapnia in fresh water. 1191 Oct 75

Exposure of rats to hyperoxia before organ harvesting protected their isolated hearts against global ischaemia-reperfusion injury in a previous study. The present study investigates whether hyperoxia influences vasomotor function and regional ischaemia of the heart. Isolated rings of the thoracic aorta were obtained from rats immediately or 24 h after in vivo exposure to 60 min of hyperoxia (>95% O2), and the in vitro dose-response to phenylephrine (PHE), prostaglandin F2alpha (PGF2alpha) and endothelin-1 (ET-1), acetylcholine (Ach) and sodium nitroprusside (SNP) was assessed. Hyperoxia in vivo increased the relaxation of aortic rings to Ach and SNP, while it delayed contraction to PHE. The effect was more evident when the vessels were harvested immediately rather than 24 h after hyperoxic exposure. In separate experiments rat hearts were isolated immediately after hyperoxia, buffer-perfused, and subjected to 30 min of regional ischaemia and reperfused for 120 min. Infarct size was determined by triphenyl tetrazolium chloride staining. Hyperoxia significantly reduced infarct size. In normoxic controls 23.0 +/- 8.3% of the area at risk was infarcted, while in hyperoxic animals infarct size was 14.8 +/- 5.6% of the area at risk (P = 0.012). Exposure of rats to hyperoxia modifies the vasomotor response of isolated aortic rings, and reduces the infarct size of isolated rat heart. These novel aspects of hyperoxic treatment require further studies to explore the potential of its clinical application.
...
PMID:Exposure of rats to hyperoxia enhances relaxation of isolated aortic rings and reduces infarct size of isolated hearts. 1216 66

The purpose of the present study was to compare the effect of 24 h of exposure to 7% O2 (normal middle ear physiological conditions) vs. 21% O2 (found in the middle ear after ventilation tube placement) on transepithelial Na+ absorption and Cl- secretion in cultured gerbil middle ear epithelial cell monolayers. Although no difference in apical Na+ absorption was identified, the UTP-induced stimulation of apical Cl- secretion in the presence of apical Na+ channel blockade with amiloride was significantly enhanced after exposure to 21% O2 compared with 7% O2 exposure. In the presence of a calcium-activated Cl- channel inhibitor, DIDS, UTP-induced stimulation of Cl- secretion after 21% O2 exposure was decreased, suggesting a role for calcium-activated Cl- channels in middle ear Cl- secretion in response to relative hyperoxia.
...
PMID:The effect of changes in ambient oxygen concentration on the bioelectric properties of middle ear mucosa. 1276 Sep 6

Supplementary oxygen is commonly administered in current medical practice. However, attention has recently been drawn to the potentially disadvantageous hemodynamic consequences in certain patients. Possible mechanisms underlying the cardiovascular responses to acute hyperoxia are unclear. The effects of acute oxygen administration on heart rate, blood pressure, cardiac output, systemic vascular resistance, and baroreflex sensitivity were studied in a series of randomised, placebo-controlled studies in healthy individuals, using validated, non-invasive techniques. The effects of oxygen administration on forearm blood flow responses to locally administered acetylcholine, an endothelium-dependent vasodilator, sodium nitroprusside, an endothelium-independent vasodilator, and l-NG-monomethylarginine, a nitric oxide synthase inhibitor, were studied using venous occlusion plethysmography. Oxygen administration for 1 hour caused a reduction in heart rate (P < 0.01) and cardiac index (P < 0.05), and an increase in mean arterial pressure (P < 0.01), systemic vascular resistance (P < 0.05), large artery stiffness (P < 0.05), and baroreflex sensitivity (P < 0.05). There were no effects on vascular responses in the isolated forearm bed. These findings indicate that oxygen administration causes acute effects on cardiovascular function, which might be important in the context of acute illness.
...
PMID:Cardiovascular effects of acute oxygen administration in healthy adults. 1288 29

Exercise-induced arterial hypoxaemia is defined as a reduction in the arterial O2 pressure (PaO2) by more than 1 kPa and/or a haemoglobin O2 saturation (SaO2) below 95%. With blood gas analyses ideally reported at the actual body temperature, desaturation is a consistent finding during maximal ergometer rowing. Arterial desaturation is most pronounced at the end of a maximal exercise bout, whereas the reduction in PaO2 is established from the onset of exercise. Exercise-induced arterial hypoxaemia is multifactorial. The ability to maintain a high alveolar O2 pressure (PAO2) is critical for blood oxygenation and this appears to be difficult in large individuals. A large lung capacity and, in turn, diffusion capacity seem to protect PaO2. A widening of the PAO2-PaO2 difference does indicate that a diffusion limitation, a ventilation-perfusion mismatch and/or a shunt influence the transport of O2 from alveoli to the pulmonary capillaries. An inspired O2 fraction of 0.30 reduces the widened PAO2-PaO2 difference by 75% and prevents a reduction of PaO2 and SaO2. With a marked increase in cardiac output, diffusion limitation combined with a fast transit time dominates the O2 transport problem. Furthermore, a postexercise reduction in pulmonary diffusion capacity suggests that the alveolo-capillary membrane is affected. An antioxidant attenuates oxidative burst by neutrophilic granulocytes, but it does not affect PaO2, SaO2 or O2 uptake (VO2), and the ventilatory response to maximal exercise also remains the same. It is proposed, though, that increased concentration of certain cytokines correlates to exercise-induced hypoxaemia as cytokines stimulate mast cells and basophilic granulocytes to degranulate histamine. The basophil count increases during maximal rowing. Equally, histamine release is associated with hypoxaemia and when the release of histamine is prevented, the reduction in PaO2 is attenuated. During maximal exercise, an extreme lactate spill-over to blood allows pH decrease to below 7.1 and according to the O2 dissociation curve this is critical for SaO2. When infusion of sodium bicarbonate maintains a stable blood buffer capacity, acidosis is attenuated and SaO2 increases from 89% to 95%. This enables exercise capacity to increase, an effect also seen when O2 supplementation to inspired air restores arterial oxygenation. In that case, exercise capacity increases less than can be explained by VO2 and CaO2. Furthermore, the change in muscle oxygenation during maximal exercise is not affected when hyperoxia and sodium bicarbonate attenuate desaturation. It is proposed that other organs benefit from enhanced O2 availability, and especially the brain appears to increase its oxygenation during maximal exercise with hyperoxia.
...
PMID:Arterial desaturation during exercise in man: implication for O2 uptake and work capacity. 1461 55

Alveolar epithelial beta-adrenergic receptor (betaAR) activation accelerates active Na+ transport in lung epithelial cells in vitro and speeds alveolar edema resolution in human lung tissue and normal and injured animal lungs. Whether these receptors are essential for alveolar fluid clearance (AFC) or if other mechanisms are sufficient to regulate active transport is unknown. In this study, we report that mice with no beta1- or beta2-adrenergic receptors (beta1AR-/-/beta2AR-/-) have reduced distal lung Na,K-ATPase function and diminished basal and amiloride-sensitive AFC. Total lung water content in these animals was not different from wild-type controls, suggesting that betaAR signaling may not be required for alveolar fluid homeostasis in uninjured lungs. Comparison of isoproterenol-sensitive AFC in mice with beta1- but not beta2-adrenergic receptors to beta1AR-/-/beta2AR-/- mice indicates that the beta2AR mediates the bulk of beta-adrenergic-sensitive alveolar active Na+ transport. To test the necessity of betaAR signaling in acute lung injury, beta1AR-/-/beta2AR-/-, beta1AR+/+/beta2AR-/-, and beta1AR+/+/beta2AR+/+ mice were exposed to 100% oxygen for up to 204 hours. beta1AR-/-/beta2AR-/- and beta1AR+/+/beta2AR-/- mice had more lung water and worse survival from this form of acute lung injury than wild-type controls. Adenoviral-mediated rescue of beta2-adrenergic receptor (beta2AR) function into the alveolar epithelium of beta1AR-/-/beta2AR-/- and beta1AR+/+/beta2AR-/- mice normalized distal lung beta2AR function, alveolar epithelial active Na+ transport, and survival from hyperoxia. These findings indicate that betaAR signaling may not be necessary for basal AFC, and that beta2AR is essential for the adaptive physiological response needed to clear excess fluid from the alveolar airspace of normal and injured lungs.
...
PMID:Upregulation of alveolar epithelial active Na+ transport is dependent on beta2-adrenergic receptor signaling. 1501 30

Paraganglia resembling the carotid body have been described in the superior laryngeal nerve (SLN) of the rat and the aim of the present study was to determine if this tissue is chemosensitive. We developed a novel isolated SLN preparation superfused with HEPES-buffered Tyrode solution at 35 degrees C in vitro. A glass suction microelectrode was used to record the electrical activity of single SLN units and a micropipette was used to pressure-eject small volumes of sodium cyanide (NaCN; 250-500 ng in 5 microl) near glomus tissue located at the main bifurcation of the SLN. The duration of the NaCN response and the number of spikes evoked after application of NaCN were compared in normoxia and hyperoxia (PO2 > 300 mmHg). Hyperoxia significantly reduced the duration and spike number of the NaCN response and a negative linear correlation existed between PO2 and response duration. In addition, hypoxia (PO2 < 60 mmHg) triggered SLN firing. Therefore, we can conclude that the paraganglia of the SLN are not only morphologically similar to the carotid body but are also excited by similar stimuli.
...
PMID:Arterial chemoreceptors in the superior laryngeal nerve of the rat. 1523 64

Newborn children can be exposed to high oxygen levels (hyperoxia) for hours to days during their medical and/or surgical management, and they also can have poor myocardial function and hemodynamics. Whether hyperoxia alone can compromise myocardial function and hemodynamics in the newborn and whether this is associated with oxygen free radical release that overwhelms naturally occurring antioxidant enzymes leading to myocardial membrane injury was the focus of this study. Yorkshire piglets were anesthetized with pentobarbital sodium (65 mg/kg), intubated, and ventilated to normoxia. Once normal blood gases were confirmed, animals were randomly allocated to either 5 h of normoxia [arterial Po(2) (Pa(O(2))) = 83 +/- 5 mmHg, n = 4] or hyperoxia (Pa(O(2)) = 422 +/- 33 mmHg, n = 6), and myocardial functional and hemodynamic assessments were made hourly. Left ventricular (LV) biopsies were taken for measurements of antioxidant enzyme activities [superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT)] and malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) as an indicator of oxygen free radical-mediated membrane injury. Hyperoxic piglets suffered significant reductions in contractility (P < 0.05), systolic blood pressure (P < 0.03), and mean arterial blood pressure (P < 0.05). Significant increases were seen in heart rate (P < 0.05), whereas a significant 11% (P < 0.05) and 61% (P < 0.001) reduction was seen in LV SOD and GPx activities, respectively, after 5 h of hyperoxia. Finally, MDA and 4-HNE levels were significantly elevated by 45% and 38% (P < 0.001 and P = 0.02), respectively, in piglets exposed to hyperoxia. Thus, in the newborn, hyperoxia triggers oxygen free radical-mediated membrane injury together with an inability of the newborn heart to upregulate its antioxidant enzyme defenses while impairing myocardial function and hemodynamics.
...
PMID:Hyperoxia causes oxygen free radical-mediated membrane injury and alters myocardial function and hemodynamics in the newborn. 1527 98

Pulmonary oedema results from an imbalance between the forces driving fluid into the airspace and the biological mechanisms for its removal. In mice lacking the alpha-subunit of the amiloride-sensitive sodium channel (alphaENaC(-/-)), impaired sodium transport-mediated lung liquid clearance at birth results in neonatal death. Transgenic expression of alphaENaC driven by a cytomegalovirus (CMV) promoter (alphaENaC(-/-)Tg+) rescues the lethal pulmonary phenotype, but only partially restores respiratory sodium transport in vitro. To test whether this may also be true in vivo, and to assess the functional consequences of this defect on experimental pulmonary oedema, we measured respiratory transepithelial potential difference (PD) and alveolar fluid clearance (AFC), and quantified pulmonary oedema during experimental acute lung injury in these mice. Both respiratory PD and AFC were roughly 50% lower (P < 0.01) in alphaENaC(-/-)Tg+ than in control mice. This impairment was associated with a significantly larger increase of the wet/dry lung weight ratio in alphaENaC(-/-)Tg+ than in control mice, both after exposure to hyperoxia and thiourea. Moreover, the rate of resolution of thiourea-induced pulmonary oedema was more than three times slower (P < 0.001) in alphaENaC(-/-)Tg+ mice. alphaENaC(-/-)Tg+ mice represent the first model of a constitutively impaired respiratory transepithelial sodium transport, and provide direct evidence that this impairment facilitates pulmonary oedema in conscious freely moving animals. These data in mice strengthen indirect evidence provided by clinical studies, suggesting that defective respiratory transepithelial sodium transport may also facilitate pulmonary oedema in humans.
...
PMID:Defective respiratory amiloride-sensitive sodium transport predisposes to pulmonary oedema and delays its resolution in mice. 1530 80

<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>