Oxygen Utilization and Toxicity in the Lungs

Fisher, Aron B.; Forman, Henry Jay

doi:10.1002/cphy.cp030105

Cited by 9 publications

(5 citation statements)

References 155 publications

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“…Oxygen toxicity appears to arise from certain metabolic products of oxygen in the form of reactive oxygen species (11). However, studies in recent years have suggested that reactive oxygen species also play an important role as signal transduction molecules within certain oxygen-sensing pathways (1, 8, 35).…”

Section: Possible Mechanisms Underlying the Changes In Respiratory Comentioning

confidence: 99%

Changes in respiratory control in humans induced by 8 h of hyperoxia

Ren

Fatemian

Robbins

2000

Journal of Applied Physiology

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In humans, 8 h of isocapnic hypoxia causes a progressive rise in ventilation associated with increases in the acute ventilatory responses to hypoxia (AHVR) and hypercapnia (AHCVR). To determine whether 8 h of hyperoxia causes the converse of these effects, three 8-h protocols were compared in 14 subjects: 1) poikilocapnic hyperoxia, with end-tidal PO(2) (PET(O(2))) = 300 Torr and end-tidal PCO(2) (PET(CO(2))) uncontrolled; 2) isocapnic hyperoxia, with PET(O(2)) = 300 Torr and PET(CO(2)) maintained at the subject's normal air-breathing level; and 3) control. Ventilation was measured hourly. AHVR and AHCVR were determined before and 0.5 h after each exposure. During isocapnic hyperoxia, after an initial increase, ventilation progressively declined (P < 0.01, ANOVA). After exposure to hyperoxia, 1) AHVR declined (P < 0.05); 2) ventilation at fixed PET(CO(2)) decreased (P < 0.05); and 3) air-breathing PET(CO(2)) increased (P < 0.05); but 4) no significant changes in AHCVR or intercept were demonstrated. In conclusion, 8 h of hyperoxia have some effects opposite to those found with 8 h of hypoxia, indicating that there may be some "acclimatization to hypoxia" at normal sea-level values of PO(2).

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Section: Possible Mechanisms Underlying the Changes In Respiratory Comentioning

confidence: 99%

Changes in respiratory control in humans induced by 8 h of hyperoxia

Ren

Fatemian

Robbins

2000

Journal of Applied Physiology

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“…Viability of fetal cultures appeared to be improved by the addition of ascorbic acid and glutathione's constituent amino acids to the culture medium. These substances may act as oxygen radical scavengers [23]. Alternatively, they may function as prooxidants, which generate radicals and cause the selection of a population of cells that is resistant to high oxygen concentrations, and may also induce the activity of protective enzymes in these cells.…”

Section: Liiscussionmentioning

confidence: 99%

Effects of Hyperoxia on Surfactant Morphology and Cell Viability in Organotypic Cultures of Fetal Rat Lung

Loo

Smith

Lykke

1989

Experimental Lung Research

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Effects of hyperoxia in an organotypic model consisting of well-differentiated fetal rat type 2 pneumocytes have been studied by light and electron microscopy. In cultures exposed to 50% oxygen for 48 h, hyperoxia caused necrosis of cultured lung cells derived from 18- to 19-day gestation fetal rats, less damage in cells derived from 20- to 21-day gestation fetal rats, and no detectable damage of cells derived from newborn rats. After exposure to hyperoxia in organotypic cultures cocultured with fibroblast monolayers, ultrastructural abnormalities of surfactant (large lamellar bodies with disordered lamellae and abnormal shape) were detected in cells from 18- to 19-day gestation fetuses. These abnormalities were not noted when fibroblast monolayers were absent. Fibroblast conditioned medium from fibroblasts exposed to hyperoxia did not cause significant surfactant abnormalities at the ultrastructural level. These changes were less marked in cultures incubated with glutathione's constituent amino acids and with ascorbic acid during exposure to hyperoxia, and in cultures pretreated with dexamethasone (20 nM) before exposure to hyperoxia.

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“…15,23,27,28,55 Although the mechanisms leading up to pulmonary hyperoxic injury are not fully understood, it is widely believed that the deleterious effects of high O 2 are the result of increased formation of reactive oxygen species (ROS), which at high concentrations cause various cytotoxic effects. 26,29,30,34,37,40,54 Presently, there are no known effective ways to mitigate the toxic side effects of O 2 therapy.…”

Section: Introductionmentioning

confidence: 99%

Distribution of Capillary Transit Times in Isolated Lungs of Oxygen-Tolerant Rats

et al. 2010

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Rats pre-exposed to 85% O2 for 5–7 days tolerate the otherwise lethal effects of 100% O2. The objective was to evaluate the effect of rat exposure to 85% O2 for 7 days on lung capillary mean transit time (t̄c) and distribution of capillary transit times (hc(t)). This information is important for subsequent evaluation of the effect of this hyperoxia model on the redox metabolic functions of the pulmonary capillary endothelium. The venous concentration vs. time outflow curves of fluorescein isothiocyanate labeled dextran (FITC-dex), an intravascular indicator, and coenzyme Q1 hydroquinone (CoQ1H2), a compound which rapidly equilibrates between blood and tissue on passage through the pulmonary circulation, were measured following their bolus injection into the pulmonary artery of isolated perfused lungs from rats exposed to room air (normoxic) or 85% O2 for 7 days (hyperoxic). The moments (mean transit time and variance) of the measured FITC-dex and CoQ1H2 outflow curves were determined for each lung, and were then used in a mathematical model [Audi et al. J. Appl. Physiol. 77: 332–351, 1994] to estimate t̄c and the relative dispersion (RDc) of hc(t). Data analysis reveals that exposure to hyperoxia decreases lung t̄c by 42% and increases RDc, a measure hc(t) heterogeneity, by 40%.

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Oxygen Utilization and Toxicity in the Lungs

Cited by 9 publications

References 155 publications

Changes in respiratory control in humans induced by 8 h of hyperoxia

Changes in respiratory control in humans induced by 8 h of hyperoxia

Effects of Hyperoxia on Surfactant Morphology and Cell Viability in Organotypic Cultures of Fetal Rat Lung

Distribution of Capillary Transit Times in Isolated Lungs of Oxygen-Tolerant Rats

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