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

The effect of hyperoxia on the Ca2+ dependence of stimulated superoxide anion radical (O2-.) production (the respiratory burst) of rat alveolar macrophages was investigated. Enhancement of the concanavalin A (con A)-stimulated respiratory burst by extracellular Ca2+ was suppressed by O2 exposure. Similarly, the inhibitory effect of verapamil on the con A-stimulated respiratory burst was reduced by O2 exposure. O2 exposure also inhibited con A stimulation that was independent of Ca2+ entry. Exposure to O2 also caused a decline in O2-. production stimulated by either A23187 or phorbol myristate acetate (PMA). With A23187 stimulation, extracellular Ca2+ was essential for either air-exposed (control) or O2-exposed cells. With PMA, stimulation was independent of extracellular Ca2+ for either air or O2-exposed macrophages and verapamil did not inhibit. Free intracellular Ca2+ concentration ([Ca2+]i) was measured in control and O2-exposed alveolar macrophages. Hyperoxic exposure did not alter [Ca2+]i in unstimulated cells. In controls, con A stimulated an immediate increase in [Ca2+]i followed by a rapid decrease and a second rise and fall. The second elevation was suppressed by verapamil or ethyleneglycol-bis (beta-aminoethylether)-N,N'-tetraacetic acid or O2 exposure. The results of both the respiratory burst assays and measurement of con A-stimulated changes in [Ca2+]i suggest that Ca2+ entry involved in stimulus-response coupling is suppressed in cellular O2 toxicity.
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PMID:Hyperoxia alters effect of calcium on rat alveolar macrophage superoxide production. 300 90

This study investigated the response of bovine pulmonary artery endothelial cells to incubation in hyperoxia (95% O2-5% CO2). Changes in cell number and morphology, release of lactate dehydrogenase, and production of arachidonic acid metabolites were assessed during continuous exposure of confluent endothelial monolayers to air (air-5% CO2, "controls") or O2 (95% O2-5% CO2, "O2-exposed") for periods of 12-72 h. Control monolayer cell numbers remained constant (approximately 2,000,000 cells/flask), whereas the number of cells in O2-exposed monolayers decreased progressively to 30% of controls (P less than 0.01) by 72 h. As assessed by radioimmunoassay, both control and O2-exposed cells produced the prostacyclin metabolite, 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), and prostaglandin F2 alpha (PGF2 alpha), but no thromboxane metabolite (TxB2) was detected. The O2-exposed cells released significantly more 6-keto-PGF1 alpha and PGF2 alpha than control cells when apparent net production rates over the entire 72-h period were compared. In addition, both control and O2-exposed (48 h) endothelial monolayers released immunoreactive leukotriene B4 (LTB4) on stimulation with calcium ionophore (10 microM A23187). As with the cyclooxygenase products, O2-exposed cells released more immunoreactive LTB4 than did controls. Both cyclooxygenase and lipoxygenase metabolites of arachidonic acid are released by cultured endothelial cells during the development of O2 toxicity.
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PMID:Production of arachidonic acid metabolites by endothelial cells in hyperoxia. 301 13

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)
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PMID:Procoagulant activity in bronchoalveolar lavage in the adult respiratory distress syndrome. Contribution of tissue factor associated with factor VII. 368 50

Heart muscle necroses can be produced in rabbits by normobaric hyperoxia. The pathogenesis of these lesions is controversial. In our investigations we found that such necroses can be prevented by beta blockers, but not by a calcium antagonist. This can be explained by the different action of the two drugs on the coronary arteries. The result supports the view that heart muscle necroses after normobaric hyperoxia are a direct toxic effect of oxygen on the heart muscle fibers.
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PMID:Heart muscle necroses following normobaric hyperoxia: modification by beta-blocking agents and calcium antagonists. 614 63

Plasma ionic status and renal excretion of acidic equivalents and electrolytes were continuously monitored in the freshwater rainbow trout (Salmo gairdneri) during 24 h normoxia (PIO2 = 120-150 torr; control); 72 h hyperoxia (PIO2 = 500-600 torr), and 24 h return to normoxia. Plasma [Cl-] progressively declined in approximate equivalence to the rise in [HCO-3] which compensated the respiratory acidosis of hyperoxia, while [Na+] increased only slightly. [Ca2+] and [K+] rose, [phosphate] declined, and [NH+4] was unchanged. During normoxic recovery, the [Na+], [Cl-] and [HCO-3] changes were reversed, [K+] and [Ca2+] showed further elevations, and [NH+4] increased sharply . Renal acid output increased greatly during hyperoxia with elevations in both NH+4 and titratable components, though the latter predominated due to a marked elevation of phosphate excretion. Renal efflux rates of other electrolytes were generally homeostatic for ECF composition, with increased Na+, K+, and Ca2+ effluxes, and decreased Cl- efflux. Clearance calculations indicated that net tubular reabsorption increased for Cl-, fell for Na+ and K+, and changed over to marked net secretion for phosphate, while net ammonia secretion increased. Most trends were reversed upon return to normoxia. The critical role of phosphate in urinary electrolyte balance and acid-base regulation is emphasized. The net renal excretion of acidic equivalents accounted for only 7-10% of the total compensation observed for the whole animal during hyperoxia. The kidney contributed primarily in conserving ECF HCO-3 and secondarily in balancing branchial exchanges.
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PMID:The mechanisms of acid-base and ionoregulation in the freshwater rainbow trout during environmental hyperoxia and subsequent normoxia. II. The role of the kidney. 672 70

Hemolymph acid-base variables (pH, PCO2 and CCO2), hemolymph Ca2+ and Na+ concentrations, and osmolality were measured in unrestrained crabs, Cancer productus, before, during and following 4 hr emersion and 43 hr hyperoxia (460-510 Torr), both at 10 degrees C. Emersion and hyperoxia provoked an acidosis associated with elevation of hemolymph CCO2 and PCO2, yet attempts to calculate PCO2 from measured pH and CCO2 always resulted in values greater than those measured directly. This discrepancy between measured and calculated PCO2, was associated with base excess, and was eliminated upon in vitro equilibration of the hemolymph and more slowly in vivo, suggesting that metabolic compensation for the acidosis occurred more rapidly than could acid-base equilibration. During emersion, increases of CCO2 and [Ca2+] provide evidence that the internal CaCO3 stores, possibly from the exoskeleton, were mobilized during acid-base compensation. Hyperoxia provoked no such increase in Ca2+, and branchial uptake of HCO3- may make a major contribution to the elevation of CCO2 during hyperoxia. It is suggested that shell buffering by aquatic crustaceans provides a means of compensation for acidosis under conditions during which branchial function is impaired.
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PMID:Non-equilibrium acid-base status in C. productus: role of exoskeletal carbonate buffers. 678 8

The effects of calcium concentration changes in carotid body cells on the chemoreceptor discharges were studied in vitro on carotid bodies removed from anaesthetized rabbits. Addition of calcium-containing liposomes to the superfusing medium increased the chemoreceptors' discharges. This effect was abolished by hyperoxia or when EGTA-containing liposomes were simultaneously added with the calcium-containing liposomes. A histological control with ferritin-enriched liposomes showed that the liposome content was transferred into the cellular elements of the preparation except the nerve endings. Results suggest a relationship between calcium concentration changes in carotid body cells and chemoafferent activity.
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PMID:Effects of ion-containing liposomes upon the chemoafferent activity of the rabbit carotid body superfused in vitro. 684 3

The rapidity and extent of hypoxic relaxation of vascular smooth muscle (VSM) from different systemic vessels is relevant to the study of mechanisms of vasodilation in different vascular beds. Variations between sites may also assist understanding of the link between oxygen tension and mechanical activity, which has been shown not to be a simple deprivation of aerobic processes. Strips of rat portal vein (RPV), rabbit ear artery (REA) and rabbit common carotid artery (RCC) were studied under isotonic conditions, contracted by 10(-6) noradrenaline (NA). Reduction of Po2 to less than 3KPa during NA constraction led to relaxation which was rapid and 90% complete in RPV, rapid and 60% in REA: the relaxation began when tissue Po2 was decreasing and was not lower than 5.5 K Pa. RCC responded slowly and only some strips relaxed. The rapidity and magnitude of relaxation for each type of vessel was comparable to that produced by removal of external calcium. Also for any one type of VSM the response to NA was abolished or diminished to a similar extent by preliminary exposure to hypoxia, or by preliminary removal of calcium. Preliminary hypoxia diminished 50 mmol.1(-1) K+ contractions as much as it diminished NA contractions. Preliminary 1-2 hour exposure to hyperoxia diminished the subsequent relaxant effect of hypoxia. Inhibition of glycolysis (iodoacetic acid) had no effect on normoxic NA contraction or on hypoxic relaxation, but prevented or diminished the subsequent recovery on reoxygenation. Low oxygen tension appears to act in VSM as though it interferes with net influx or utilisation of external calcium.
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PMID:Responses of systemic vascular smooth muscle to hypoxia. 690 37

Nifedipine is a potent slow channel calcium antagonist and systemic vasodilator recently reported to attenuate hypoxic pulmonary vasoconstriction in man. Other systemic vasodilators have also been shown to attenuate hypoxic pulmonary vasoconstriction, but their effects in some species may be mediated by reflex beta-adrenergic discharge. We evaluated the effect of nifedipine on the relation between pulmonary arterial pressure and blood flow during hyperoxia (inspired partial pressure of oxygen [PO2] 200 mm Hg) and hypoxia (inspired PO2 50 mm Hg) in denervated ventilated pig lungs perfused in situ with the animal's own blood. Ten lungs were ventilated with alternating 15 minute periods of hyperoxia and hypoxia. Hypoxia shifted the pulmonary artery pressure (x axis)-blood flow (y axis) relationship to the right and decreased its slope, indicating vasoconstriction. Nifedipine, given as a 0.1, 1, or 10 microgram/kg bolus into the pulmonary artery, caused a dose-dependent reduction of hypoxic pulmonary vasoconstriction. It is concluded that nifedipine is a potent pulmonary vasodilator acting locally within the lung and that it might be useful in the therapy of hypoxic pulmonary hypertension from chronic lung disease in man.
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PMID:Inhibition of hypoxic pulmonary vasoconstriction by nifedipine. 712 46

Oxygen exposure for a sufficient duration at high partial pressure results in pulmonary edema in humans and animals. Although the specific mediators of oxygen toxicity are unknown, evidence suggests that oxygen-based radicals such as superoxide anion (O2.) are increased in the lungs in the presence of hyperoxia and contribute to this injury. A series of isomeric prostanoid compounds, the isoprostanes, are formed by the free radical-initiated lipid peroxidation of arachidonic acid (AA). One of these isomers, 8-iso-PGF2alpha, is elevated in the bronchial alveolar lavage fluid of rats exposed to 90% oxygen for 48 h and is associated with a significant increase in protein accumulation in the pulmonary extravascular space. Alveolar macrophages (AMs) are capable of producing large quantities of (O2.), suggesting a role in pulmonary oxygen toxicity. We hypothesized that isolated rat AMs exposed to hyperoxia generate increased amount of 8-iso-PGF2alpha. AMs were exposed to air or 90% oxygen for 6, 12, 24, 48, 72, 96, and 120 h in the absence and presence of AA and/or calcium ionophore (A23187) and 8-iso-PGF2alpha was measured in the culture media. Exposure of primary cultures of AMs to 90% oxygen resulted in a significant increase in 8-iso-PGF2alpha in the media (25 +/- 2 pg/mL) compared with air-exposed controls (14 +/- 1 pg/mL). The addition of 10 microM AA and 2 microM A23187 to the culture media resulted in a marked increase in 8-iso-PGF2alpha production by AMs exposed to air and 90% oxygen. However, treatment of AMs with the combination of AA and A23187, followed by exposure to 90% oxygen for 72 h, resulted in a 27-fold increase in 8-iso-PGF2alpha compared with media alone and 90% oxygen. AMs metabolized free and phospholipid-bound AA to 8-iso-PGF2alpha, an activity enhanced in the 90% oxygen environment. Finally, acetylsalicylic acid, a cyclooxygenase inhibitor and free radical scavenger, reduced but did not abolish production of 8-iso-PGF2alpha. This study provides evidence that AMs produce a free radical-mediated isomeric prostaglandin compound that may be involved in pulmonary oxygen toxicity.
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PMID:8-ISO-PGF2alpha production by alveolar macrophages exposed to hyperoxia. 956 55


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