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

This study investigates the respiratory physiology of bioluminescent larvae of Pyrearinus termitilluminans in relation to their tolerance to hypoxia and hyperoxia and to the supply of oxygen for bioluminescence. The partial pressure of oxygen (P(O2)) was measured within the bioluminescent prothorax by in vivo electron paramagnetic resonance (EPR) oximetry following acclimation of larvae to hypoxic, normoxic and hyperoxic (normobaric) atmospheres and during periods of bioluminescence (during normoxia). The P(O2) in the prothorax during exposure to an external P(O2) of 15.2, 160 and 760 mmHg was 10.3+/-2.6, 134+/-0.9 and 725+/-73 mmHg respectively (mean +/- s.d., N=5; 1 mmHg=0.1333 kPa). Oxygen supply to the larvae via gas exchange through the spiracles, measured by determining the rate of water loss, was also studied in the above atmospheres and was found not to be dependent upon P(O2). The data indicated that there is little to no active control of extracellular tissue P(O2) within the prothorax of these larvae. The reduction in prothorax P(O2) observed during either attack-response-provoked bioluminescence or sustained feeding-related bioluminescence in a normoxic atmosphere was variable, but fell within the range 10-25 mmHg. The effect of hypoxic atmospheres on bioluminescence was measured to estimate the intracellular P(O2) within the photocytes of the prothorax. Above a threshold value of 50-80 mmHg, bioluminescence was unaffected by P(O2). Below this threshold, an approximately linear relationship between P(O2) and bioluminescence was observed. Taken together with the extracellular P(O2) measurements, this suggests that control of P(O2) within the photocyte may occur. This work establishes that EPR oximetry is a valuable technique for long-term measurement of tissue P(O2) in insects and can provide valuable insights into their respiratory physiology. It also raises questions regarding the hypothesis that bioluminescence can have a significant antioxidative effect by reduction of prothorax P(O2 )through oxygen consumption.
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PMID:Measurement of oxygen partial pressure, its control during hypoxia and hyperoxia, and its effect upon light emission in a bioluminescent elaterid larva. 1048 22

Using dynamic Magnetic Resonance Imaging (dMRI), blood-brain barrier (BBB) permeability (k(PSrho)) and tissue interstitial leakage space (v(e)) were evaluated in zinc-deficient (ZnDF) male weanling Wistar rats following 3 days exposure to hyperoxia (85% O2). Temporal monitoring of T1-weighted MR image changes, following a bolus intravenous injection of gadolinium-DTPA, allowed estimation of BBB integrity. Three-day exposure of hyperoxia caused a marginal loss of BBB integrity, reflected in a slight increase in kPSrho and v(e), observed in both the animals fed adequate zinc (ZnAL) and pair-fed controls (ZnPF). However, zinc deficiency resulted in a significant increase in both kPSrho and v(e), indicating a severely disturbed BBB. In addition MR-visible free water was elevated in ZnDF brains following hyperoxia treatment indicating that a loss of BBB integrity may be associated with neuronal edema. The diminished BBB integrity may be free-radical mediated as the ratio of oxidized to reduced glutathione (GSSG:GSH) was significantly elevated.
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PMID:Zinc deficiency exacerbates loss in blood-brain barrier integrity induced by hyperoxia measured by dynamic MRI. 1065 21

Oreochromis alcalicus grahami is a small cichlid fish that lives in shallow peripheral lagoons of Lake Magadi, Kenya. The internal surface of the air-bladder is highly vascularized, illustrating possible utilization as an accessory respiratory organ. The wall of the bladder consists of five distinct tissue layers. From the outer to the inner surfaces are: a squamous, undifferentiated epithelial cell; a collagen-elastic tissue space; a smooth muscle tissue band; an inner connective tissue space; and columnar gas-gland cells projecting into the lumen. The cell membrane over the perikarya of the gas-gland cells was sporadically broken. The disruptions were ascribed to possible physical damage by discharging gas-bubbles. Juxtaluminally, the gas-gland cells attached across tight junctions. The cells have highly euchromatic nuclei and conspicuously large intracytoplasmic secretory bodies. On the blood capillary facing (basal) aspect, the cell membrane of the gas-gland cells is highly amplified. The cells insert onto a smooth muscle tissue band. The morphological features and the topographical arrangement of the gas-gland cells in O. a. grahami are indicative of an operative exchange of materials between them and the underlying tissue components especially the blood capillaries. For a fish that subsists in hot, highly saline and alkaline water heavily invested by avian predators and where the partial pressure of oxygen diurnally shifts from virtual anoxia to hyperoxia, development of a versatile air-bladder for efficient buoyancy control conforms to the functional demands placed on it by a unique environment. Illustratively, instead of the gas-gland morphology in O. a. grahami resembling that in the freshwater fishes, the group from which the fish has evolved, it compares more closely to that of the marine fish. This similarity suggests amazing parallel evolutionary adaptation to biophysically corresponding aquatic milieus.
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PMID:Functional morphology of the gas-gland cells of the air-bladder of Oreochromis alcalicus grahami (teleostei: cichlidae): an ultrastructural study on a fish adapted to a severe, highly alkaline environment. 1085 97

Nitric oxide (NO), a pro-oxidant gas, is used with hyperoxia (O(2)) to treat neonatal pulmonary hypertension and recently bronchopulmonary dysplasia, but great concerns remain regarding NO's potential toxicity. Based on reports that exposure to oxidant gases results in pulmonary extracellular matrix injury associated with elevated lavage fluid levels of extracellular matrix components, we hypothesized that inhaled NO with or without hyperoxia will have the same effect. We measured alveolar septal width, lung collagen content, lavage fluid hydroxyproline, hyaluronan and laminin levels in neonatal piglets after 5 days' exposure to room air (RA), RA + 50 ppm NO (RA + NO), O(2) (FiO(2) > 0.96) or O(2) + NO. Matrix metalloproteinase (MMP) activity and MMP-2 mRNA were also measured. In recovery experiments, we measured lung collagen content in piglets exposed to RA + NO or O(2) + NO and then allowed to recover for 3 days. The results show that lung collagen increased 4-fold in the RA + NO piglets, the O(2) and O(2) + NO groups had only a 2-fold elevation relative to RA controls. Unlike the RA + NO piglets, the O(2) and O(2) + NO groups had more than 20-fold elevation in lung lavage fluid hydroxyproline compared to the RA group. O(2) and O(2) + NO also had increased lung MMP activity, extravascular water, and lavage fluid proteins. MMP-2 mRNA levels were unchanged. After 3 days' recovery in room air, the RA + NO groups' lung collagen had declined from 4-fold to 2-fold above the RA group values. The O(2) + NO group did not decline. Alveolar septal width increased significantly only in the O(2) and O(2) + NO groups. We conclude that 5 days' exposure to NO does not result in pulmonary matrix degradation but instead significantly increases lung collagen content. This effect appears potentially reversible. In contrast, hyperoxia exposure with or without NO results in pulmonary matrix degradation and increased lung collagen content. The observation that NO increased lung collagen content represents a new finding and suggests NO could potentially induce pulmonary fibrosis.
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PMID:High-dose inhaled nitric oxide and hyperoxia increases lung collagen accumulation in piglets. 1104 69

Because it was still uncertain whether a stimulation of beta1-adrenoceptors accelerated alveolar fluid clearance in hyperoxic lung injury, the effect of denopamine, a selective beta1-adrenergic agonist, on alveolar fluid clearance was determined in rats exposed to 93% oxygen for 48 and 56 h. Alveolar fluid clearance was measured by the progressive increase in the concentration of Evans blue labeled albumin instilled into the alveolar spaces over 1 h at 37 degrees C in isolated rat lungs. The principle results were as follows: 1) Although lung water volume increased in rats exposed to hyperoxia for 48 and 56 h, basal alveolar fluid clearance did not change for up to 56 h; 2) Denopamine increased alveolar fluid clearance in rats exposed to hyperoxia as well as in rats without exposure to hyperoxia; 3) Denopamine primarily increased amiloride-insensitive alveolar fluid clearance in rats exposed to hyperoxia; 4) The potency of denopmaine was similar to that of terbutaline, a selective beta2-adrenergic agonist. In summary, denopamine is a potent stimulator of alveolar fluid clearance in rats exposed to hyperoxia.
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PMID:Beta1-adrenergic agonist is a potent stimulator of alveolar fluid clearance in hyperoxic rat lungs. 1128 98

The objective of this study was to determine whether endogenous nitric oxide (NO), specifically the inducible NO synthase isoform (iNOS: NOS II), reduces or amplifies lung injury in mice breathing at a high oxygen tension. Previous studies have shown that exogenous (inhaled) NO protects against hyperoxia-induced lung injury, and that endogenous NO derived from iNOS inhibits leukocyte recruitment and protects against lung injury induced by lipopolysaccharide. In the present study, hyperoxia (> 98% O(2) for 72 h) induced acute lung injury in both wild-type and iNOS-deficient mice as determined by elevated albumin and lactate dehydrogenase levels in bronchoalveolar lavage fluid (BALF) and by increased extravascular lung water. Lung injury was greater in iNOS-deficient mice than in wild-type mice and was associated with an increased number of polymorphonuclear leukocytes in BALF. iNOS messenger RNA expression levels increased in the lungs of wild-type hyperoxic mice. Nitrotyrosine, a marker of reactive NO species, was expressed in both wild-type and iNOS-deficient mice in hyperoxia, indicating an iNOS-independent pathway for protein nitration. We conclude that iNOS is capable of reducing pulmonary leukocyte accumulation and lung injury. The data indicate that iNOS induction serves as a protective mechanism to minimize the effects of acute exposure to hyperoxia.
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PMID:Antiinflammatory properties of inducible nitric oxide synthase in acute hyperoxic lung injury. 1130 31

Immaturity and oxygen toxicity have been implicated in the pathogenesis of the neonatal disease bronchopulmonary dysplasia. The present study aimed to investigate the use of magnetic resonance imaging (MRI) to assess hyperoxia-mediated lung injury in the term and premature neonate. Term (gestation, 22 d) and premature (21 d) rat pups were exposed to hyperoxia (>95%) or air for a 6-d period (n = 7) and assessed for lung damage by MRI. Pulmonary signal intensities of T1-weighted images were significantly increased in both hyperoxia-exposed term and premature neonates, relative to air-breathing controls (p < 0.01). T2-weighted MRI signal intensities were also greater in premature and term rat pups exposed to hyperoxia, but failed to reach significance (p > 0.05). Elevated MRI pulmonary signal intensities may have represented an increase in magnetic resonance-detectable free water, possibly indicating an increase in edema. Corresponding histologic evidence of lung injury was detected in both term and premature rat pups exposed to hyperoxia. Histologic samples indicated focal regions of alveolar hemorrhage, immune cell infiltration, edema, and collapse in both term and premature rat neonates exposed to hyperoxia. Alveolar air space was assessed (n = 5) by light microscopy within a 0.5 mm2 region of the superior left and inferior right pulmonary lobes of each treatment group. Alveolar area of the superior left lung lobe of the premature hyperoxia treatment group was significantly smaller than other treatment groups (p < 0.05). Reduced area for respiratory exchange was probably a result of observed focal areas of edema and collapse. MRI-detectable increases in lung signal intensity may have represented an increase in hyperoxia-induced pulmonary edema in the 6-d-old rat neonate. Increases in signal intensity correlated with the appearance of edema in pulmonary histologic samples. Premature delivery had a less defined effect on lung injury but possibly exacerbated hyperoxia-mediated pulmonary damage.
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PMID:Magnetic resonance imaging of pulmonary damage in the term and premature rat neonate exposed to hyperoxia. 1156 94

To elucidate the influence of oxidative stress on the brain functions during aging, the cognitive performance ability of rats was assessed by using the water-maze test as an oxidative stress before and after hyperoxia. Young rats showed significantly greater learning ability than both old rats and vitamin-E-deficient rats. Although the memory functions of all rats were Impaired after oxidative stress, the memory retention of young rats was greater than those of other groups. After the stress, none of the rats recovered their learning ability. During aging and through hyperoxia, the release of acetylcholine from nerve terminals was remarkably decreased. Instead, thiobarbituric acid reactive substance (TBARS) contents in rat hippocampus and cebral cortex, and their synaptic membranes, were significantly increased during aging and by oxidative stress. The antioxidative defense system in rat brain was also changed by the stress. These results suggest that oxidative stress may contribute to learning and memory deficits following oxidative brain damage during aging.
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PMID:Impairment of learning and memory in rats caused by oxidative stress and aging, and changes in antioxidative defense systems. 1179 7

Heart rate and dive behaviour were monitored in double-crested cormorants (Phalacrocorax auritus) during shallow (1 m) and deep diving (12 m), after breathing different gas mixtures, to investigate the role of depth and the accompanying changes in blood gas levels in cardiac and behavioural control during voluntary diving. Pre-dive heart rate in both shallow- and deep-diving birds was approximately three times the resting heart rate (137.9+/-17.5 beats min(-1); mean +/- S.D., N=5), falling abruptly upon submersion to around 200-250 beats min(-1). During shallow diving, the initial reduction in heart rate was followed by a secondary, more gradual decline, to around the resting level. In contrast, during deep diving, heart rate stabilised at 200-250 beats min(-1). In dives of similar duration, mean dive heart rate was significantly lower during shallow diving (163.2+/-14.0 beats min(-1)) than during deep diving (216.4+/-7.7 beats min(-1)), but in both cases was significantly above the resting value. The difference in cardiac response is probably due to an increase in arterial oxygen tension (Pa(O(2))) during the descent phase of deep dives (compression hyperoxia). Exposure to a hyperoxic gas mixture before shallow diving significantly increased mean dive heart rate, while exposure to a hypoxic gas mixture in both the shallow and deep dive tanks significantly reduced mean dive heart rate. In contrast, breathing hypercapnic gas before diving had no significant effect on dive heart rate. We suggest that the cardiac response to voluntary diving in double-crested cormorants is strongly influenced by changes in blood oxygen levels throughout the dive. Dive duration was unaffected by alterations in inspired gas composition, but surface interval duration decreased during hyperoxic gas exposure and increased during hypoxic gas exposure. The most efficient dive pattern (highest dive/pause ratio) was observed after hyperoxic exposure. Our study suggests that blood oxygen level is a powerful stimulus that facilitates the cardiac and behavioural adjustments during foraging that are important components of a strategy allowing double-crested cormorants to maximise the time spent under water and, hence, potential foraging time.
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PMID:The effects of depth on the cardiac and behavioural responses of double-crested cormorants (Phalacrocorax auritus) during voluntary diving. 1180 82

Changes in branchial vacuolar-type H(+)-ATPase B-subunit mRNA and Na+, K(+)-ATPase alpha- and beta-subunit mRNA and ATP hydrolytic activity were examined in smolting Atlantic salmon exposed to hyperoxic and/or hypercapnic fresh water. Pre-smolts, smolts, and post-smolts were exposed for 1 to 4 days to hyperoxia (100% O2) and/or hypercapnia (2% CO2). Exposure to hypercapnic water for 4 days consistently decreased gill vacuolar-type H(+)-ATPase B-subunit mRNA levels. Salmon exposed to hyperoxia had either decreased or unchanged levels of gill B-subunit mRNA. Combined hyperoxia + hypercapnia decreased B-subunit mRNA levels, although not to the same degree as hypercapnic treatment alone. Hyperoxia generally increased Na+, K(+)-ATPase alpha- and beta-subunit mRNA levels, whereas hypercapnia reduced mRNA levels in presmolts (beta) and smolts (alpha and beta). Despite these changes in mRNA levels, whole tissue Na+, K(+)-ATPase activity was generally unaffected by the experimental treatments. We suggest that the reduced expression of branchial vacuolar-type H(+)-ATPase B-subunit mRNA observed during internal hypercapnic acidosis may lead to reduction of functional V-type H(+)-ATPase abundance as a compensatory response in order to minimise intracellular HCO3- formation in epithelial cells.
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PMID:Vacuolar-type H(+)-ATPase and Na+, K(+)-ATPase expression in gills of Atlantic salmon (Salmo salar) during isolated and combined exposure to hyperoxia and hypercapnia in fresh water. 1191 Oct 75


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