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

To explore the role of the glutathione oxidation-reduction cycle in altering the sensitivity of rats to the effects of hyperbaric hyperoxia, we administered N,N-bis(2-chloroethyl)-N-nitrosourea (BCNU) to decrease tissue glutathione reductase activity. We then exposed these animals and their matched vehicle-treated controls to 100% O2 at 4 ATA. Animals that received BCNU and were immediately exposed to hyperbaric O2 showed enhanced toxicity by seizing earlier in the exposure than controls. Animals that received BCNU 18 h before the hyperbaric O2 exposure were paradoxically protected from the effects of the exposure with a prolongation of their time to initial seizure and a marked increase in their survival time during the exposure. Tissue glutathione concentrations were also measured in the various groups and the hyperbaric O2 exposure produced marked decreases in hepatic glutathione levels in all control animals. In animals treated with BCNU 18 h before exposure, hepatic glutathione concentrations also decreased, but the concentrations had significantly increased during the 18-h waiting period, allowing these animals to maintain hepatic levels in the normal range even during their hyperbaric exposures. We conclude that treatment of rats with BCNU 18 h before exposure to hyperbaric hyperoxia results in enhanced protection of the animals during the exposure.
J Appl Physiol (1985) 1988 Dec
PMID:BCNU-induced protection from hyperbaric hyperoxia: role of glutathione metabolism. 321 53

Preexposure to hypoxia increased survival and lung reduced glutathione-to-oxidized glutathione ratios (GSH/GSSG) and decreased pleural effusions in rats subsequently exposed to continuous hyperoxia. In addition, lungs from hypoxia-preexposed rats developed less acute edematous injury (decreased lung weight gains and lung lavage albumin concentrations) than lungs from normoxia-preexposed rats when isolated and perfused with hydrogen peroxide (H2O2) generated by xanthine oxidase (XO) or glucose oxidase (GO). In contrast, when perfused with elastase or exposed to a hydrostatic left atrial pressure challenge, lungs isolated from hypoxia-preexposed rats developed the same acute edematous injury as lungs from normoxia-preexposed rats. The mechanism by which hypoxia preexposure conferred protection against H2O2 appeared to depend on hexose monophosphate shunt (HMPS)-dependent increases in lung glutathione redox cycle activity. First, before perfusion with GO, lungs from hypoxia-preexposed rats had increased glutathione peroxidase and glucose 6-phosphate dehydrogenase (but not catalase or glutathione reductase) activities compared with lungs from normoxia-preexposed rats. Second, after perfusion with GO, lungs from hypoxia-preexposed rats had increased H2O2 reducing equivalents, as reflected by increased GSH/GSSG and NADPH/NADPH+, compared with lungs from normoxia-preexposed rats. Third, pretreatment of rats with an HMPS inhibitor, (6-aminonicotinamide) or a glutathione reductase inhibitor, [1,3-bis(2-chloroethyl)-1-nitrosourea] prevented hypoxia-conferred protection against H2O2-mediated acute edematous injury in isolated lungs. These findings suggest that increased detoxification of H2O2 by glutathione redox cycle and HMPS-dependent mechanisms contributes to tolerance to hyperoxia and resistance to H2O2 of lungs from hypoxia-preexposed rats.
J Appl Physiol (1985) 1988 Dec
PMID:Hypoxia increases glutathione redox cycle and protects rat lungs against oxidants. 321 62

Breathing 87% O2 for 7 days causes pulmonary vascular remodeling and pulmonary hypertension in the rat. In the isolated perfused lung of the normal and O2-exposed rat, change in pre- and postcapillary resistance was determined in response to challenge with angiotensin II (ANG II; 5, 25, and 50 micrograms) or histamine (0.5 and 1.0 microgram). In the hyperoxic lung both pre- and postcapillary resistance were increased at base line, although the latter less consistently so. In response to each agent precapillary resistance increased more than postcapillary resistance in the hyperoxic lung. In the normal lung pre- and postcapillary reactivity to histamine were similar but the latter was the greater in response to ANG II. In the hyperoxic lung only the pre- and postcapillary response to the first challenge of ANG II (5 micrograms) was greater than normal. The magnitude of the precapillary response was not related to the level of base-line resistance, and this response was significantly increased in a small number of hyperoxic lungs with base-line resistance in the normal range. Tachyphylaxis occurred after the first dose of ANG II. In the hyperoxic lung only the precapillary response to 0.5 micrograms histamine was greater than normal. We conclude that exposure to hyperoxia for 7 days causes an increase in pulmonary arterial reactivity. Furthermore, the alteration in reactivity is not caused by vascular restriction. We hypothesize that it is attributable to peripheral extension of smooth muscle in alveolar wall arteries.
J Appl Physiol (1985) 1988 Dec
PMID:Pulmonary vascular reactivity in hyperoxic pulmonary hypertension in the rat. 321 63

Exposure of adult animals to 48-72 h of 100% O2 breathing is associated with a blunting of hypoxic pulmonary vasoconstriction (HPV) (Newman et al. J. Appl. Physiol. 54: 1379-1386, 1983). It is unknown whether HPV is also diminished in neonates after hyperoxic exposure and if so to what extent such suppression might interfere with pulmonary gas exchange during hypoxic gas breathing. We tested the possibility that hyperoxia would suppress HPV and interfere with ventilation-perfusion (VA/Q) matching and therefore gas exchange in neonatal piglets. Twelve 2- to 4-wk-old piglets were exposed for an average of 68 h to greater than 90% inspired O2. A control group of eight piglets was exposed to room air for a similar period of time. Immediately after exposure the animals were anesthetized and instrumented. Pulmonary hemodynamics and respiratory and inert gas exchange were assessed while the animals inspired an O2 fraction of 1.0, 0.21, and 0.12. After 20 min of hypoxic gas breathing, pulmonary arterial pressure rose to a lesser degree in the hyperoxia (H)-exposed animals than in the control (C) animals (P less than 0.02). The increase in pulmonary vascular resistance was similarly blunted. Venous admixture of the insoluble inert gas, sulfur hexafluoride, an index of extremely low VA/Q areas, was increased during hypoxic gas breathing compared with room air breathing in the H-preexposed animals (P less than 0.02). Standard deviation of pulmonary blood flow was increased (P less than 0.02), indicating an increase in mismatching of VA/Q during hypoxic breathing in the H-preexposed animals compared with the C animals.(ABSTRACT TRUNCATED AT 250 WORDS)
J Appl Physiol (1985) 1987 Dec
PMID:Effects of hyperoxia on vasoconstriction and VA/Q matching in the neonatal lung. 343 85

1. The ventilatory responses to step changes from rest to 100 W cycling exercise were studied in five healthy human subjects. Exercise was performed in hypoxia (end-tidal O2 pressure, PET,O2, 50-55 mmHg), a condition characterized by a marked enhancement of arterial chemoreceptor activity, and in hyperoxia (PET,O2 greater than 250 mmHg), a condition in which arterial chemoreceptor activity is largely suppressed. The subjects were studied at each O2 level after placebo and after an oral dose of 120 mg propranolol. 2. The magnitude of phase 1, the immediate, rapid ventilatory response at the onset of work, was unaffected by hypoxia and at both oxygen levels it was also unaffected by propranolol. 3. Phase 2, analysed from 20 to 120 s after the onset of exercise, was significantly affected by both O2 level and beta-blockade. The kinetics of the ventilatory changes in this phase were well described in all four conditions by a simple exponential function. The overall mean time constants after placebo were shorter in hypoxia (31.0 s) than in hyperoxia (40.2 s), and at each O2 level longer after propranolol, in hypoxia 61.3 s and in hyperoxia 106.0 s. 4. Continuous analysis of gas sampled at the mouth with a mass spectrometer showed constancy of end-tidal PCO2 throughout the step change in hypoxia both with and without beta-blockade. In contrast, in both hyperoxic conditions PET,CO2 rose, mainly in phase 2, to a value 5-6 mmHg higher than the starting value. 5. The steady-state ventilation was higher in hypoxia than in hyperoxia, and end-tidal CO2 pressure, PET,CO2, correspondingly lower. Neither ventilation nor PCO2 were, however, affected by propranolol in either condition. 6. It is concluded that the arterial chemoreceptors are important for both the rate of adaptation of ventilation to a new rate of metabolism during a step change of work rate, and for the matching of ventilation to CO2 flow which normally ensures isocapnia. The further slowing of the dynamics of the ventilatory response in hyperoxia as well as the preserved isocapnia in hypoxia after beta-blockade argue against any major role of beta-adrenergic mechanisms for these functions of the arterial chemoreceptors. The observed effects are considered to be secondary to the reduced cardiac output and an increased CO2 storage initially during exercise following beta-adrenergic blockade.
J Physiol 1987 Dec
PMID:Effects of beta-adrenergic blockade on the ventilatory responses to hypoxic and hyperoxic exercise in man. 344 3

A new suction catheter, designed to deliver alternately oxygen or suction, prevented episodes of hypoxia and hyperoxia in a group of infants during endotracheal suctioning. Twenty infants received both conventional endotracheal suctioning and suctioning by the new catheter. The infants had a maximal change from a presuctioning transcutaneous oxygen (PtcO2) of 12 +/- 8 torr and required 3.1 +/- 2 min to regain their presuctioning oxygenation level compared to a maximal change of 21 +/- 10 torr (p less than .05) and a stabilization time of 5.3 +/- 2.6 min (p less than .05) in the conventionally treated group. Three study infants experienced an abnormal PtcO2 (either less than 40 or greater than 90 torr), while 13 control infants suffered these abnormalities (p less than .01). The use of this new suction device effectively reduced the exposure of this group of infants to episodes of aberrant oxygen states and allowed for a shorter recovery time.
Crit Care Med 1987 Dec
PMID:Prevention of hypoxia and hyperoxia during endotracheal suctioning. 347 94

Alveolar fibrin deposition commonly occurs in the lungs of patients with the adult respiratory distress syndrome (ARDS). Bronchoalveolar lavage (BAL) from patients with ARDS, control patients with interstitial lung disease (ILD), congestive heart failure, or exposure to hyperoxia, and normal healthy subjects was studied to determine whether local alterations in procoagulant activity favor alveolar fibrin deposition in the lungs in ARDS. Procoagulant activity capable of shortening the recalcification time of plasma deficient in either factor VII or factor VIII was observed in unconcentrated BAL of all patients, but was significantly greater in BAL from patients with ARDS when compared with that of control subjects (p less than 0.001). Unconcentrated BAL from patients with ARDS shortened the recalcification time of plasma deficient in factor X, but no functional thrombin was detectable. BAL procoagulant from patients with ARDS was inhibited by concanavalin A, an inhibitor of tissue factor. The hydrolysis of purified human factor X by BAL from the ARDS and other patient groups was determined by measuring the amidolytic activity of generated factor Xa on its N-benzoyl-L-isoleucyl-L-glutamyl-glycyl-L-arginine-p-nitroanilide substrate. The procoagulant activity of BAL was associated with the development of amidolytic activity, indicating activation of factor X. BAL from patients with ARDS contained more factor X activating activity than did BAL from control groups (p less than 0.001). This activity was calcium dependent and was maximal at 1 mM ionized calcium. The BAL factor X activating activity was most active at neutral pH and was sedimented by ultracentrifugation at 100,000 x g.(ABSTRACT TRUNCATED AT 250 WORDS)
Am Rev Respir Dis 1987 Dec
PMID:Procoagulant activity in bronchoalveolar lavage in the adult respiratory distress syndrome. Contribution of tissue factor associated with factor VII. 368 50

The bronchiolar epithelium of rats is anatomically immature at birth. We now ask whether postnatal hyperoxia impairs the normal development of bronchiolar epithelium; and, if development is impaired, is the impairment permanent? To answer these questions, we exposed newborn rats to hyperoxia (greater than 95% O2, 1 atm) or air for 7 days and killed the rats at age 7 or 30 days. We used ultrastructural and morphometric means to assess maturation of the bronchiolar epithelium. Hyperoxia substantially diminished the postnatal increase in nuclear numerical density of bronchiolar Clara cells and ciliated cells. Hyperoxia also markedly delayed the rise in volume density of Clara cell secretory granules and rough endoplasmic reticulum but accelerated the increase in volume density of Clara and ciliated cell mitochondria. When rats exposed to hyperoxia from age 1 to 7 days were thereafter allowed to breathe air, by age 30 days all the differences were eliminated that were detected between the air- and O2-breathing groups at age 7 days. We conclude hyperoxia causes a marked but nonpermanent suppression of maturation of the bronchiolar epithelium.
Am J Physiol 1986 Dec
PMID:Hyperoxia reversibly suppresses development of bronchiolar epithelium. 378 92

The partition of O2 uptake between gills and skin was examined in the freshwater eel (Anguilla anguilla L.) at ambient PO2 ranging from hyperoxia (PO2 = 400 Torr) to severe hypoxia (PO2 = 10 Torr), using a technique of open-flow respirometry. All the expired water was collected, and the ventilatory flow and the mixed expired water PO2 were directly measured. The ventilatory water flow decreased moderately in hyperoxia, increased markedly between normoxia and 40 Torr, and below 40 Torr, hyperventilation was gradually reduced. Between PO2 400 and 70 Torr, the total O2 uptake was constant and the skin O2 uptake was lower than gill O2 uptake (32% of total uptake in normoxia). Between 70 and 10 Torr, the skin contribution to the total O2 uptake progressively increased, and was higher than gill O2 uptake in severe hypoxia. A possible facilitation of cutaneous O2 uptake in hypoxia is discussed from estimates of the O2 diffusing capacity of the skin.
Respir Physiol 1986 Dec
PMID:Cutaneous and gill O2 uptake in the European eel (Anguilla anguilla L.) in relation to ambient PO2, 10-400 Torr. 379 48

Although oxygen therapy has been used in the care of critically ill patients for many years, the recognition of pulmonary oxygen toxicity as an important clinical problem is relatively recent. The biochemical basis of oxygen toxicity is increased production of highly reactive, partially reduced metabolites of oxygen, including hydrogen peroxide and free radicals, by cells in hyperoxia. Enzymatic intracellular defense mechanisms exist which protect cells from the toxic effects of oxygen free radicals. The physiologic manifestations of oxygen toxicity include decreases in vital capacity, diffusing capacity, and lung compliance. The pathologic changes of oxygen toxicity are not specific and resemble those of the adult respiratory distress syndrome. Many drugs used in the care of patients, including bleomycin, nitrofurantoin, and corticosteroids, may exacerbate oxygen-induced lung injury. No effective pharmacologic means exist for lessening pulmonary oxygen toxicity in humans.
Chest 1985 Dec
PMID:Pulmonary oxygen toxicity. 390 87


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