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

Lung macrophages (LM) play a crucial role in pulmonary bacterial defense. High inspired oxygen concentrations are used in a variety of diseases and "oxygen toxicity" could impair antibacterial function. We therefore examined the effect of sustained in vitro hyperoxia on LM bactericidal function, and on generation of two bactericidal oxygen metabolites. The LM were cultivated under aerobic (PO2 approximately 140 mmHg) or hyperoxic (PO2 approximately 630 mmHg) conditions for 48 h, and then incubated with Staphylococcus aureus labeled with 3H thymidine for 30 min. Incubated monolayers were processed for measurement of total bacterial uptake and for number of viable intracellular bacteria. Superoxide anion (O2-) and hydrogen peroxide (H2O2) generation was determined in similarly cultivated cells stimulated with opsonized zymosan. The results indicate that the bacterial killing capacity of oxygen-cultivated LM is significantly decreased (p less than 0.001). In addition, a significant (p less than 0.001) decrease in generation of O2- and H2O2 was noted after exposure to high oxygen tensions. The data suggest that decreased bactericidal function after sustained hyperoxia may be due to an impairment of a specific bactericidal mechanism, i.e., an impaired "respiratory burst."
Am Rev Respir Dis 1983 Sep
PMID:Decreased bactericidal function and impaired respiratory burst in lung macrophages after sustained in vitro hyperoxia. 631 Oct 64

Bovine pulmonary artery endothelial cells in culture were exposed for up to 7 d to a gas mixture containing 80% O2, 5% CO2, and 15% N2 (hyperoxia) and were compared by phase contrast and electron microscopy to cells exposed to a gas mixture containing 20% O2, 5% CO2, and 75% N2. Cells exposed to hyperoxia became enlarged and showed vacuolization and increased lysosomes within 24 to 48 h. These changes were progressive over the 7 d period of exposure. Between 3 and 7 d of exposure to hyperoxia the cells showed reductions in polysomes and endoplasmic reticulum. Despite the other marked cytoplasmic changes, the appearance of mitochondria of oxygen-exposed cells remained unchanged from those of air-exposed cells throughout the 7 d period. Preconfluent and confluent cells responded qualitatively similarly to hyperoxia, but morphological evidence of injury occurred more rapidly for preconfluent cells. We conclude that the initial early structural injury of the endothelial cell exposed to hyperoxia occurs in lysosomes and that the mitochondrial structure is relatively resistant to injury.
In Vitro 1983 Sep
PMID:Ultrastructural changes in bovine pulmonary artery endothelial cells exposed to 80% O2 in vitro. 641 90

The effect of sleep state on ventilatory rhythmicity following graded hypocapnia was determined in two normal subjects and one patient with a chronic tracheostomy. Passive positive-pressure hyperventilation (PHV) was performed for 3 min awake and during nonrapid-eye-movement (NREM) sleep with hyperoxia [fractional inspired O2 concentration (FIO2) = 0.50], normoxia and hypoxia (FIO2 = 0.12). During wakefulness, no immediate posthyperventilation apnea was noted following abrupt cessation of PHV in 27 of 28 trials [mean hyperventilation end-tidal CO2 partial pressure (PETCO2) 29 +/- 2 Torr, range 22-35]. During spontaneous breathing in hyperoxia, PETCO2 rose from 40.4 +/- 0.7 Torr awake to 43.2 +/- 1.4 Torr during NREM sleep. PHV during NREM sleep caused apnea when PETCO2 was reduced to 3-6 Torr below NREM sleep levels and 1-2 Torr below the waking level. In hypoxia, PETCO2 increased from 37.1 +/- 0.1 awake to 39.8 +/- 0.1 Torr during NREM sleep. PHV caused apnea when PETCO2 was reduced to levels 1-2 Torr below NREM sleep levels and 1-2 Torr above awake levels. Apnea duration (5-45 s) was significantly correlated to the magnitude of hypocapnia (range 27-41 Torr). PHV caused no apnea when isocapnia was maintained via increased inspired CO2. Prolonged hypoxia caused periodic breathing, and the abrupt transition from short-term hypoxic-induced hyperventilation to acute hyperoxia caused apnea during NREM sleep when PETCO2 was lowered to or below the subject's apneic threshold as predetermined (passively) by PHV. We concluded that effective ventilatory rhythmogenesis in the absence of stimuli associated with wakefulness is critically dependent on chemoreceptor stimulation secondary to PCO2-[H+].
J Appl Physiol Respir Environ Exerc Physiol 1983 Sep
PMID:Interaction of sleep state and chemical stimuli in sustaining rhythmic ventilation. 641 11

Ventilatory regulation of intact, unrestrained lugworms Arenicola marina living in glass-tube artificial burrows was examined for values of inspired seawater PO2, PIO2, from 20 to 700 torr, at constant ambient pH and PCO2 values. The water ventilation rate and the respiratory characteristics of the ventilated seawater were measured. The water convection requirement and the corresponding specific rates of O2 uptake and CO2 production were calculated. The mean ventilatory water flow was a complex function of PIO2: decrease in hyperoxia, increase in hypoxia, decrease in extreme hypoxia. Compared to the normoxic responses, hyperoxia led to a hypercapnia (and acidosis) and moderate hypoxia to a hypocapnia (and alkalosis) in the expired water, variations which presumably reflect blood acid-base balance changes. Thus, as in other water breathers, the regulation of the organism's oxygenation may override the regulation of its acid-base balance. The lugworm's oxygen exchanger is highly efficient. However, below a critical partial pressure, PIO2 ca 120 torr, values of O2 consumption and ventilation decreased. A second critical O2 partial pressure appeared at PIO2 values between 80 and 40 torr; a 'switch-on' of anaerobic metabolism. These phenomena may be viewed as features of an adaptative respiratory strategy selected for in relation with the lugworm's particular peristaltic ventilatory mechanism and its intertidal mode of life.
Respir Physiol 1984 Sep
PMID:Ventilation and respiratory gas exchanges of the lugworm Arenicola marina (L.) as functions of ambient PO2 (20-700 torr). 644 Dec 15

Exposure of cultured bovine pulmonary artery endothelial cells to hyperoxia (95% O2) caused cellular injury manifested by decreased growth rates and release of cytoplasmic lactic dehydrogenase (LDH). In addition, a greater number of polymorphonuclear leukocytes (PMN) adhered to endothelial cells that had been exposed to hyperoxia for 24 or 48 h than to control endothelial cells that had been exposed to normoxia (15% O2). Direct endothelial cell injury from hyperoxia may contribute to vascular damage and the increased PMN accumulation seen in lungs of animals exposed to hyperoxia.
Am Rev Respir Dis 1983 Sep
PMID:Hyperoxia damages cultured endothelial cells causing increased neutrophil adherence. 661 40

In decerebrate, vagotomized, paralyzed, and ventilated cats, phrenic and respiratory-related hypoglossal discharges were evident at normocapnic normoxia or hyperoxia. Both increased progressively in hypercapnia or hypoxia. With increasing drive, onset of inspiratory hypoglossal activity began earlier relative to phrenic onset; an early expiratory hypoglossal burst was also observed. Following subanesthetic doses of chloralose, halothane, ketamine, or pentobarbital, hypoglossal activity was depressed much more than phrenic discharge. In moderate hypercapnia or hypoxia, phrenic activity increased more than hypoglossal, whereas, at high drive, the latter rose more sharply in some cats. Electromyograms of the diaphragm and genioglossus were recorded in intact awake cats to determine if their responses and those of decerebrates are comparable. Respiratory-related genioglossal discharge was evident in normocapnia. We conclude that anesthesia suppresses hypoglossal motor activities much more than those of the bulbospinal-phrenic system. Data for decerebrate cats and unanesthetized cats or humans provide no evidence of a differential distribution of chemoreceptor afferents on hypoglossal and bulbospinal-phrenic neurons, as suggested by results in anesthetized animals.
J Appl Physiol Respir Environ Exerc Physiol 1983 Sep
PMID:Respiratory-related hypoglossal nerve activity: influence of anesthetics. 662 15

Permanently implanted Silastic tonometers were used to measure average extracellular oxygen tension in the medullary cavity of osteotomized rabbit tibias stabilized with external pin fixation. During uncomplicated healing the baseline bone pO2 rose slowly with time from 10 to 20 mm Hg while during staphylococcal infection pO2 varied between 8 and 15 mm Hg and showed no correlation with the healing time. The maximal response of the bone pO2 to oxygen breathing correlated linearly with the healing time whether the osteotomy was infected or not. On the 42nd day the maximal pO2 during systemic hyperoxia was 85 mm Hg for the control bones, 42 mm Hg for the osteotomized bones, and 30 mm Hg for the infected osteotomized bones. The results indicate moderate bone tissue hypoxia during uncomplicated healing and more profound hypoxia during healing affected by infection.
J Surg Res 1984 Sep
PMID:Tissue oxygen tension in externally stabilized tibial fractures in rabbits during normal healing and infection. 674 36

The influence of the depth of anaesthesia on the contribution of central and peripheral chemoreceptors to the slope of the ventilatory response to CO2 during hyperoxia was studied in 12 cats anaesthetized with chloralose-urethane or pentobarbital. By artificial perfusion of the pontomedullary region of the brainstem it was possible to assess the peripheral (Sp) and central (Sc) ventilatory sensitivity to CO2, as well as to vary selectively the level of anaesthesia at the ponto-medullary region (central level) or the overall level. In each cat Sp and Sc were assessed at the initial and at one or two deeper anaesthetic levels. Going from the initial to deeper anaesthetic levels both Sp and Sc decreased. However, Sp/Sc did not change significantly, whether the overall or the central level of anaesthesia was increased. Also the B-value, i.e. the PaCO2 of the extrapolated ventilation-PaCO2 curve at zero ventilation, did not change significantly when going to deeper anaesthetic levels. It is concluded that the respiratory depression caused by the anaesthetics used is due to an influence on the respiratory integrating centres, central chemoreceptors, or both.
Respir Physiol 1980 Sep
PMID:Influence of the depth of anaesthesia on the peripheral and central ventilatory CO2 sensitivity during hyperoxia. 677 64

This paper describes alterations in the incidence of cleft lip and palate in CL/Fr mice subsequent to experimental manipulation of maternal respiratory oxygen levels during a critical period of pregnancy. Only a few previous studies have shown that the incidence of some "genetically determined" malformations in mammals can be decreased by environmental procedures. In addition to demonstrating a decreased incidence of cleft lip and palate subsequent to maternal hyperoxia on gestational days 10 and 11 in a genetically susceptible strain, the results of the present study show that hypoxia at this time increases the incidence of cleft lip and palate.
Proc Natl Acad Sci U S A 1981 Sep
PMID:Hyperoxia and hypoxia in pregnancy: simple experimental manipulation alters the incidence of cleft lip and palate in CL/Fr mice. 694 11

Cochlear microcirculation was studied with oxygen-sensitive microelectrodes simultaneously in all three scalas during anoxia, hyperoxia, and hypercapnia. The anoxia caused a sharp decline of Po2 in the scala media (SM), scala vestibuli (SV), and scala tympani (ST). Hyperoxia and hypercapnia resulted in an elevation of Po2 in all three scalas. During anoxia, the SM showed the earliest and largest decline in Po2, with the shortest recovery and reoxygenation time. When Po2 slopes (during anoxia) were compared, the SM to ST and the SM to SV were substantially different and remained different even when the partial pressures of oxygen quantified as oxygen in nanomoles. Our experiments also showed that changes in Po2 within the SM closely correlate with changes of endocochlear potential and BP.
Arch Otolaryngol 1982 Sep
PMID:Perilymphatic and endolymphatic PO2. Variations during anoxia, hyperoxia, and hypercapnia. 698 2


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