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)

The study is based on the hypothesis that lung endothelial cell permeability increases in 100% oxygen and predates the appearance of microscopically visible interstitial edema. Rats were exposed to either 100% oxygen or air in a chamber. Endogenous albumin was used as an index of permeability and measured by electron microscopic colloidal gold linked immunocytochemistry, quantified by systematic random methods. Albumin staining was expressed as relative albumin concentration (RAC), the ratio of gold particles (x 100) per point counted (gp.10(2)/pt) relating to each component. The RAC in lung perivascular/peribronchial interstitial ground substance after 24 h of hyperoxia was five times more than that of rats exposed to air for the same interval. The median value (interquartile ranges) for the oxygen-exposed group was 92.4 (39.5, 149.6) gp. 10(2)/pt compared with 14.7 (6.6, 25.9) gp. 10(2)/pt for the air-exposed group. After 60 h of 100% oxygen, the RAC was 103.4 (65.5, 148.9) gp. 10(2)/pt (60-h air exposed RAC was 11.6 (8.7, 60.4) gp. 10(2)/pt), no different from 24-h exposures. These results suggest that there was a significant leak of albumin to the perivascular/peribronchial interstitium by 24 h of exposure to 100% oxygen, which would indicate endothelial cell permeability to albumin increases earlier than has previously been reported.
 ...
PMID:Lung capillary albumin leak in oxygen toxicity. A quantitative immunocytochemical study. 808 53

We investigated the effects of lung edema protein on ventilatory mechanics with special reference to surfactant activity. The edema fluid was obtained from hyperoxia-exposed adult rabbits. In immature newborn rabbits that could not be artificially ventilated at an insufflation pressure of 25 cm H2O, mean tidal volumes of > 27 ml/kg were obtained by supplementation with a natural surfactant (S-alone) or natural surfactant mixed with lung edema fluid (EF), the edema protein-to-surfactant ratio of which was < or = 5.6. A mixture with a ratio of 11.2 (11.2-EF/S), however, decreased the volume to 10.9 ml/kg (P < 0.05 vs S-alone). Surfactant mixed with isolated albumin at a concentration equal to that in 11.2-EF/S decreased the tidal volume to 8.6 ml/kg (NS vs 11.2-EF/S), and with isolated fibrinogen lowered it to 18.1 mg/kg (P < 0.05 vs S-alone). We conclude that lung edema fluid impairs ventilation through surfactant inactivation when the protein-to-surfactant ratio increases, and that albumin and fibrinogen are the main causes of this impairment.
 ...
PMID:Impairment of surfactant activity and ventilation by proteins in lung edema fluid. 815 52

The rat erythrocytes' Na, K-ATPase activity was found to drop under the effects of five various stresses: immobilisation, hypothermia, hyperoxia, physical strain, and physical strain against the background of fasting. An endogenous digoxin-like inhibiting agent(s) acting on the Na, K-ATPase seems to appear in the blood plasma of the animals under stress. The suggestion is corroborated by the fact that albumin-less supernatants of the stressed rats' blood plasma are able to inhibit the Na, K-ATPase in the erythrocytes of the control animals.
 ...
PMID:[The dynamics and mechanism of changes in the erythrocyte Na, K-ATPase activity of rats under the action of different types of stressors]. 816 17

Neutrophil accumulation in alveolar spaces is a conspicuous finding in hyperoxia-exposed lungs. We hypothesized that xanthine oxidase (XO)-derived oxidants contribute to retention of neutrophils in hyperoxic lungs. Rats were subjected to normobaric hyperoxia (100% O2) for 48 h, and lungs were assessed for neutrophil sequestration (morphometry and lavage cell counts) and injury (lavage albumin levels and lung weights). In rats exposed to hyperoxia, we found increased (P < 0.05) lung neutrophil retention, lavage albumin levels, and lung weights compared with normoxia-exposed control rats. Suppression of XO activity by pretreatment with allopurinol decreased (P < 0.05) lung neutrophil retention but increased (P < 0.05) lavage albumin concentrations and lung weights in hyperoxic rats. Allopurinol treatment had no effect (P > 0.05) on the numbers of macrophages or lymphocytes recoverable by lung lavage. Depletion of XO activity by an independent method, tungsten feeding, also decreased (P < 0.05) lung lavage neutrophil counts and increased (P < 0.05) lavage albumin concentrations. We conclude that XO may be involved in lung neutrophil retention but not lung injury during exposure to hyperoxia.
 ...
PMID:Xanthine oxidase promotes neutrophil sequestration but not injury in hyperoxic lungs. 817 9

Active Na+ transport and lung edema clearance were studied in a model of lung injury caused by sublethal oxygen exposure. Rats exposed to 85% O2 for 7 days were studied at 0, 7, 14, and 30 days after removal from the hyperoxic chamber and compared with room air controls. In the isolated-perfused, fluid-filled rat lung, albumin flux from the perfusate into the air spaces increased after oxygen exposure and returned to control values after 7 days of recovery. However, permeability to small solutes (Na+ and mannitol) normalized only after 30 days of recovery from hyperoxia. Active Na+ transport increased immediately after oxygen exposure and returned to control values 7 days after removal from hyperoxic chamber. Na-K-adenosinetriphosphatase (ATPase) activity, and protein expression in alveolar epithelial type II cells obtained at the end of the isolated lung experiments increased significantly after the oxygen exposure compared with controls in association with the increased active Na+ transport. We conclude that active Na+ transport and lung liquid clearance are increased in the subacute hyperoxic phase of lung injury in rats, due in part to the upregulation of alveolar epithelial Na-K-ATPases. Conceivably, this behavior protects against the effects of lung injury by allowing the injured lung to clear edema more effectively. Accordingly, this upregulation may be targeted as a strategy to diminish edema in patients with lung injury.
 ...
PMID:Active sodium transport and alveolar epithelial Na-K-ATPase increase during subacute hyperoxia in rats. 820 51

In the ventilated ischemic lung, oxygen tension will increase at a time when glucose depletion may impair antioxidant defenses, thereby predisposing the lung to injury mediated by oxygen radicals. In the unventilated ischemic lung, however, glucose depletion in the setting of low oxygen tension may decrease production of ATP, leading to injury by a different mechanism. In this study, we evaluated the role of both oxygen tension and glucose concentration on ischemic injury in isolated ferret lungs. Injury, defined as an increase in vascular permeability, was assessed by measurement of filtration coefficient (Kf) and osmotic reflection coefficient for albumin (sigma alb) after 3 h of normothermic (37 degrees C) ischemia without reperfusion. Lungs were ventilated with either 95% O2-5% CO2 or 0% O2-5% CO2. The vasculature was flushed with physiological salt solution containing either 15 mM glucose (hyperoxia-glucose, anoxia-glucose), 15 mM sucrose (hyperoxia-sucrose, anoxia-sucrose), or no substrate (hyperoxia-no substrate, anoxia-no substrate) (n = 6 for each condition). Kf and sigma alb in hyperoxia-no substrate group did not differ from values in minimally ischemic normoxic normoglycemic ferret lungs. Without glucose, ischemic injury was worse in anoxic than in hyperoxic lungs. With glucose, ischemic injury was worse in hyperoxic than in anoxic lungs. Glucose exacerbated injury in hyperoxic, but not anoxic, lungs. These results indicate that ischemic injury in these lungs depended on both oxygen tension and glucose concentration and suggest that both oxygen radical generation and ATP depletion during ischemia may contribute to the development of this injury.
 ...
PMID:Effects of oxygen tension and glucose concentration on ischemic injury in ventilated ferret lungs. 822 35

To determine if recombinant human Cu-Zn superoxide dismutase (rhSOD) would prevent acute lung injury caused by hyperoxia and barotrauma, 26 newborn piglets were studied. Ten piglets were hyperventilated (arterial PCO2 15-20 Torr) with 100% O2 for 48 h. A second group received identical treatment for 4 h (n = 2) or 48 h (n = 8) but was given 5 mg/kg of rhSOD intratracheally at time 0. Six piglets were normally ventilated (arterial PCO2 40-45 Torr) for 48 h with 21% O2. Pulmonary function and tracheal aspirates were examined at time 0 and at 24 and 48 h, and bronchoalveolar lavage was performed at 48 h. In piglets treated with hyperoxia and hyperventilation, lung compliance decreased 42%, and tracheal aspirates showed an increase in neutrophil chemotactic activity (32%), total cell counts (135%), elastase activity (93%), and albumin concentration (339%) over 48 h (P < 0.05). All variables were significantly lower in rhSOD-treated piglets and comparable to normoxic control values. Surfactant remained active in all groups. Immunohistochemistry demonstrated that at 48 h significant rhSOD was distributed homogeneously in terminal airways. Adding rhSOD to tracheal aspirates of hyperoxic hyperventilated piglets did not alter neutrophil chemotaxis, suggesting that rhSOD protected the lung by reducing the production of chemotactic mediators. Results indicate that acute lung injury caused by 48 h of hyperoxia and hyperventilation is significantly ameliorated by prophylactic intratracheal administration of rhSOD.
 ...
PMID:Prophylactic effects of recombinant human superoxide dismutase in neonatal lung injury. 833 53

In order to evaluate further the physiological and inflammatory changes of meconium aspiration syndrome (MAS), 25 newborn piglets (1-2 days old, 1.5 +/- 0.4 kg) were studied. Piglets were briefly ventilated with 100% oxygen and then received an intratracheal bolus of 3 mL/kg of a 20% suspension of human meconium. They were then further ventilated, keeping PaCO2 at approximately 40 torr and PaCO2 at 70 torr during 4, 12, 24, and 48 h studies. Pulmonary function studies and tracheal aspirates were obtained at time zero and serially throughout the study. Bronchoalveolar lavage was performed at the end of the study to examine endogenous surfactant function. Control piglets received 3 mL/kg of intratracheal saline and were then ventilated for 48 h at an inspired oxygen concentration and mean airway pressure matched to the meconium treated group (to control for the effects of hyperoxia and barotrauma on the lung). MAS caused acute decreases in gas exchange and dynamic lung compliance, which returned toward baseline by 48 h (P < 0.001, ANOVA). Tracheal aspirate absolute neutrophil count, neutrophil chemotactic activity, albumin, and total protein concentrations also increased significantly over time (P < 0.001). Endogenous surfactant function appeared to be significantly inhibited by the meconium. All variables of lung injury were significantly higher in the meconium group compared to the saline control group over the 48 h study. Newborn piglets provide a clinically relevant model of MAS, demonstrating physiological and inflammatory changes with apparent alterations in endogenous surfactant function. Effective therapies for MAS may require interventions directed at all of these components of lung injury.
 ...
PMID:Meconium aspiration syndrome: physiological and inflammatory changes in a newborn piglet model. 836 15

The effects of hypoxia (95% N2/5% CO2) followed by hyperoxia (95% O2/5% CO2) were determined in isolated lungs of premature (gestational age 128 to 135 d) and full-term (postnatal age 0 to 5 d) lambs perfused with autologous blood (100 mL.min-1.kg body weight-1). In full-term lungs, hypoxia-hyperoxia compared with hypoxia alone decreased pulmonary artery pressure and increased weight gain and extravascular lung water. In premature lungs, the increase in weight gain was greater and was associated with hemorrhage and increased pulmonary arterial and peak airway pressures. Papaverine eliminated reoxygenation-induced differences in pulmonary artery pressure, peak airway pressure, and weight gain in both age groups. Osmotic reflection coefficients for total protein and albumin, measured by a modification of the filtered volume technique, averaged 0.591 +/- 0.054 (SEM) and 0.465 +/- 0.054 (SEM), respectively, and were not altered by reoxygenation or age. Catalase activity in lung tissue and erythrocytes was lower in premature lambs, but there were no age-related differences in superoxide dismutase or glutathione peroxidase activities. These results demonstrate that hypoxia-hyperoxia in isolated lamb lungs increased lung weight due to edema formation in full-term lamb lungs and hemorrhage in premature lamb lungs and that this increase was greater in premature lamb lungs. We speculate that the weight gain caused by reoxygenation was due to a vasodilation-induced increase in surface area in full-term lamb lungs and a vasoconstriction-induced increase in vascular pressure in premature lamb lungs.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Developmental differences in catalase activity and hypoxic-hyperoxic effects on fluid balance in isolated lamb lungs. 851 Oct 27

We assessed the effect of varying levels of hyperoxia on 14C-albumin flux across bovine pulmonary artery endothelial cell (BPAEC) monolayers. Endothelialized nitrocellulose filters were mounted in Ussing-type chambers which were filled with cell culture medium (M 199). Equimolar amounts of 14C-labeled and unlabeled albumin were added to the "hot" and "cold" chambers, respectively, and the monolayers were exposed to 3 hours of varying levels of oxygen (16%, 30%, 40%, 60%, and 95%). When compared to 16% O2, exposure to hyperoxic gas mixtures of 40% or greater progressively increased albumin permeability across endothelial monolayers within 3 hours to a value 2.5 times higher at 95% O2 compared to 16% O2 (p < 0.001). Hyperoxia-induced permeability increases were prevented by catalase, superoxide dismutase, desferrioxamine, and allopurinol. Our data indicate that hyperoxia induces endothelial permeability changes more rapidly than previously reported even at O2 concentrations as low as 40%.
 ...
PMID:Early albumin leakage in pulmonary endothelial monolayers exposed to varying levels of hyperoxia. 888 89


<< Previous 1 2 3 4 5 6 7 Next >>