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

Periodic breathing of the Biot or cluster type was induced in spontaneously breathing, pentobarbital anesthetized cats by placing bilateral lesions within the pneumotaxic system of the rostral pons. Control lesions positioned outside of the critical nuclei never resulted in Biot breathing. The periodic pattern was characterized by clusters of breaths which were separated by distinct periods of apnea and was clearly not of Cheyne-Stokes quality. Test gas challenges inducing hypoxia and hypercapnia tended to diminish the apneic breatholds, whereas hyperoxia potentiated the periodic breathing by increasing the duration of the non-ventilatory phase. Only hypercapnia significantly altered the tidal volume of Biot breaths by increasing the depth of breathing. No conclusions can be drawn as to whether the Biot pattern arises from an inherent central respiratory controller periodicity, or from oscillations in arterial blood gas tensions and peripheral chemoreceptor (and mechanoreceptor) inputs. It is suggested that the experimental model for Biot breathing may be of unique importance for studying the control of expiratory duration, particularly apnea. Also, it is of interest that similar breathing patterns and gas responses occur in the neonate and adult.
Respir Physiol 1981 Dec
PMID:Experimental Biot periodic breathing in cats: effects of changes in PiO2 and PiCO2. 679 61

Minute volume (V), tidal volume (VT), respiratory frequency (f), venous lactate, and clavicular air sac gas composition were measured in domestic fowl at rest and during exercise, breathing hypoxic, hyperoxic, or hypercapnic gas. Hyperoxia produced no significant change in ventilation, CO2 inhalation produced increases in V and VT, but the changes in f appeared to be related to the stage of exercise at which CO2 was administered. The sensitivity of the hypercapnic response was similar in resting and exercising birds. Compared with the effects of CO2, hypoxia elicited only a weak ventilatory response in rest and exercise conditions despite severe tissue anaerobiosis.
J Appl Physiol Respir Environ Exerc Physiol 1982 Dec
PMID:Control of ventilation in running birds: effects of hypoxia, hyperoxia, and CO2. 681 11

Pulmonary and intracardiac hemodynamic findings are reported. They were obtained by means of catheterization of right cardiac departments and the pulmonary artery with thermodilution in 57 patients with chronic nonspecific pulmonary diseases (CNPD), under conditions of resting, rationed bicycle-ergometric exercise, hypo- and hyperoxia, and nitroglycerin administration. Changes in pulmonary and intracardiac hemodynamics which reflect the ongoing exhaustion of compensatory mechanisms in the external respiration apparatus, the pulmonary vascular system and the heart, are shown to precede the formation of right ventricular hypertrophy in obstructive CNPD A classification of secondary pulmonary hypertension, based on clinical and instrumental signs, is offered.
Kardiologiia 1982 Dec
PMID:[Pulmonary hypertension in chronic nonspecific lung diseases]. 716 25

In order to determine if lungs with emphysema respond to oxygen toxicity in a different way from normal lungs, the effects of hyperoxia on pulmonary function, morphologic aspects, and survival were studied in rats with enzyme-induced emphysema. A hyperoxic pulmonary syndrome similar to adult respiratory distress syndrome (ARDS) was produced by a continuous 48-h exposure to 100% oxygen at 1 atm. An emphysematous condition was induced by intratracheal instillation of porcine pancreatic elastase. The 4 study groups consisted of (1) control, (2) oxygen-treated, (3) elastase-treated, and (4) combined oxygen-elastase-treated rats. The emphysematous rats exposed to 100% O2 had reductions in quasi-static compliance and CO diffusing capacity similar to those in oxygen-treated normal animals. They also had reductions in forced expiratory volumes and flow rates similar to those in rats treated with elastase alone. Histologically, there was no enhancement or attenuation of emphysematous or ARDS lesions in the combined oxygen-elastase lungs compared with that in lungs treated with only one agent. Emphysematous and normal rats were also exposed for 96 h to a similar hyperoxic atmosphere to evaluate survival. The survival curves for these 2 groups were not statistically different. These results indicate that the severity of ARDS alterations was not affected by the emphysematous condition, and hyperoxia did not enhance or attentuate preexisting emphysematous lesions. These findings suggest that emphysematous lungs respond to hyperoxia in a similar fashion to normal lungs, and that the functional and structural manifestations of oxygen toxicity are simply superimposed over preexisting emphysematous changes.
Am Rev Respir Dis 1982 Dec
PMID:The effects of emphysema on oxygen toxicity in rats. 718 Dec 25

The effect of hyperbaria and hyperbaric hyperoxia on the disposition kinetics of theophylline were investigated in the dog. The drug was administered as a 5 mg/kg iv bolus at 1 atmospheres absolute (ATA), 2.8 ATA and 6 ATA. Serial blood samples were collected over an eight hour period and analyzed for theophylline concentration using a gas chromatographic method. From the resultant data, elimination half-life, volume of distribution and total body clearance were calculated. There were no apparent effects of hyperbaria or hyperbaric hyperoxia on any of the parameters describing theophylline disposition, implying that, in the animal model studied, distribution, elimination and effect should remain constant.
Res Commun Chem Pathol Pharmacol 1981 Dec
PMID:Theophylline pharmacokinetics during hyperbaria and hyperbaric hyperoxia in the dog. 732 40

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.
Clin Toxicol 1981 Dec
PMID:Brain energy metabolism in mice exposed to oxygen at 1 atmosphere absolute. 733 82

Basic fibroblast growth factor (bFGF) is a mitogenic polypeptide for a wide variety of cell types and has been immunolocalized in the rodent and human lung. We investigated the mRNA and protein expression of bFGF in hyperoxic-injured adult mouse lungs using northern blot analysis and immunohistochemistry. Mice (6-8 weeks) were continuously exposed to 80% oxygen up to 4 days. Levels of bFGF mRNA were increased from room air control on days 3 and 4 of hyperoxia. mRNA levels of acidic fibroblast growth factor (aFGF), fibronectin, and transin/stromelysin were also examined in this injury model. Similar to bFGF, the fibronectin and transin/stromelysin mRNA levels were increased after 3 days of hyperoxia. In contrast, the aFGF mRNA levels were gradually reduced on each day of hyperoxia. A rabbit polyclonal anti-bFGF antibody was used to determine the distribution and levels of expression in the hyperoxic-injured lungs. The room air control and day 1 hyperoxic-exposed lungs exhibited staining for bFGF in the basement membranes of the blood vessels, airways, and alveoli. Patchy but intense alveolar staining was prominent on day 4 of hyperoxia. The bFGF immunoreactivity of blood vessels and airways was unaffected by the hyperoxia exposure. These results suggest that bFGF may play a role in the alveolar response to hyperoxic-induced injury by virtue of the altered mRNA levels and protein distribution in this injury model.
J Cell Biochem 1994 Dec
PMID:Increased expression of basic fibroblast growth factor in hyperoxic-injured mouse lung. 753 14

We compared the effects of treatment with methylprednisolone or the 21-aminosteroids, U-74389 and U-74006F (Tirilizad mesylate), on hyperoxic lung injury and the associated expression of mRNA for several adhesion molecules in rats. Inhalation of > 95% oxygen for up to 72 hr in Sprague-Dawley rats produced a marked increase in lung weight and an accumulation of fluid in the thorax when compared with air-breathing controls. Hyperoxia also induced a marked neutrophil-rich influx of inflammatory cells into the bronchial lumen as measured by bronchoalveolar lavage. Neutrophil numbers in bronchoalveolar lavage fluid peaked after 60 hr of exposure to s 95% oxygen; this was associated with a marked upregulation of mRNA for the adhesion molecules P-selectin and E-selectin but not VCAM-1. mRNA for ICAM-1 was constitutively expressed at high levels in both air-breathing controls and in the lungs of rats exposed to high concentrations of oxygen. Pretreatment with the 21-aminosteroids reduced hyperoxic lung damage and improved survival times in animals exposed to > 95% oxygen. However, treatment with methylprednisolone significantly decreased survival times. Treatment with U-74389 did not significantly (p > 0.05) inhibit the BAL neutrophilia and did not significantly (p > 0.05) reduce hyperoxia-induced increases in mRNA expression for P-selectin and E-selectin. The inhibition of hyperoxic lung damage coupled with improved survival seen in treated animals suggests that 21-aminosteroids may provide valuable treatments for pulmonary disorders in which oxidant damage has been implicated.
Environ Health Perspect 1994 Dec
PMID:Attenuation of oxidant-induced lung injury by 21-aminosteroids (lazaroids): correlation with the mRNA expression for E-selectin, P-selectin, ICAM-1, and VCAM-1. 753 86

Specific changes in composition and content of lung extracellular matrix (ECM) proteoglycans (PGs) and hyaluronan (HA) have been observed during the acute response to damage in several forms of injury including infant respiratory distress syndrome (IRDS). These ECM components are thought to modulate the healing response. Hyperoxia, a contributing factor to IRDS, is known to damage both adult and developing lung, however, the extent and pattern of impairment depends on lung maturity. We hypothesized that exposing neonatal rats to hyperoxia alone might result in changes in lung HA, as well as in age-specific changes in lung PGs, similar to those shown to occur in IRDS. In control rats, lung HA decreased over the first 10 days of life, whereas rats exposed to hyperoxia exhibited a time-dependent, time-limited increase in both lung HA and lung wet weight. Histochemistry showed the HA in hyperoxia-exposed lungs to be accumulated in perivascular cuffs of medium sized arteries, and in the alveolar walls. Rats were then exposed to normoxia or hyperoxia for 7 days beginning at either 3 days of life (neonatal) or 21 days (adolescent), and lung tissue was cultured in the presence of [35S]-sulfate to label newly synthesized PGs. Proteoglycans were extracted, and analyzed by isopycnic CsCl gradient centrifugation, sequential enzymatic deglycosylation, size chromatography, and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). When controlled for total protein extracted, 63% more label was incorporated into large molecular weight material in the tissue exposed to hyperoxia, with a 95% increase in incorporation in the most dense fraction, D1. [35S]-Sulfate incorporation into chondroitin and dermatan sulfate in hyperoxic tissue specifically increased 116% (242% in the D1 fraction), while incorporation into heparan sulfate remained essentially unchanged. There was a nearly fivefold increase in [35S]-sulfate incorporation into chondroitin sulfate chains in the D1 fraction. When the D1 fractions of extracts of treated and control rat lungs were compared on SDS-PAGE, a large chondroitin sulfate proteoglycan (CSPG; core protein of 195 kDa) was upregulated in the D1 fraction from hyperoxic tissue of neonatal rats, but was not detected in the lungs of adolescent animals exposed to hyperoxia. This CSPG and four additional large CSPGs were noted to be upregulated on western blotting by a polyclonal antibody directed against the G1 domain of the aggrecan protein core. We conclude that hyperoxia alone causes an increase in lung HA and lung water, and speculate that this contributes significantly to the clinical syndrome of IRDS. In addition, several large CSPGs are upregulated by hyperoxic exposure in a developmentally specific manner. We speculate that this increase in CSPGs may interfere with the normal developmental sequence of events, contributing to hypoalveolarization.
Am J Respir Cell Mol Biol 1995 Dec
PMID:Hyperoxia alone causes changes in lung proteoglycans and hyaluronan in neonatal rat pups. 757

A review of the effects of brain-stem transections, carbachol microinjections and lesions does not show that the pons is necessary and sufficient for paradoxical sleep (PS) generation. The different theories that explain the mechanisms of PS rebound are summarized. In some circumstances, PS rebound depends upon the stressful quality of PS deprivation. PS appears to necessitate oxidative metabolism of glucose and, in certain situations, PS may be increased by hyperoxia.
Sleep 1994 Dec
PMID:Paradoxical sleep mechanisms. 770 Dec 5


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