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

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.
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PMID:Ventilation and respiratory gas exchanges of the lugworm Arenicola marina (L.) as functions of ambient PO2 (20-700 torr). 644 Dec 15

Larval and adult bullfrogs, Rana catesbeiana (Shaw), were exposed to 28 days of normoxia (PO2 150 mmHg), hypoxia (PO2 70-80 mmHg) or hyperoxia (PO2 greater than 275 mmHg) at 20-23 degrees C, after which the following morphological measurements were made: (1) mass, thickness, capillary mesh density and blood-water barrier of the skin; (2) mass, volume, cava density and blood-gas barrier of lungs; and, for the larvae, (3) arch length, filament density and size, and blood-water barrier of the gills. Chronic hypoxia induced profound morphological changes in the gas exchange organs of larvae, but not of adults. In tadpoles, the skin became thinner, with a doubling of capillary mesh density and a having of the blood-water barrier. The gas diffusion barrier of the lungs remained unchanged, but the lung volume and density of the lung wall cava both increased significantly. The internal gills showed a marked enlargement upon hypoxic exposure, both in numbers of gill filaments and size of each filament. The blood-water barrier remained unchanged. Chronic hyperoxia, unlike chronic hypoxia, caused no significant changes in the morphology of the gas exchange organs of larvae. Chronic exposure to hypoxia or hyperoxia failed to produce any significant morphological changes in adult bullfrogs. These data indicate that the great morphological plasticity of larvae, culminating in metamorphosis, also extends to profound adjustments in the gas exchange organs when oxygen transfer becomes limited, a response lacking in adults.
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PMID:Respiration during chronic hypoxia and hyperoxia in larval and adult bullfrogs (Rana catesbeiana). I. Morphological responses of lungs, skin and gills. 660 81

We determined the effects of slow wave sleep on ventilatory compensation to inspiratory elastic loads (18 cm H2O/L). Multiple loading trials of variable duration were applied in three healthy adult humans in wakefulness and during NREM sleep. During wakefulness, ventilatory response over 5 loaded breaths were highly variable. Tidal volume (VT), mean inspiratory flow (VT/TI), and minute ventilation (VE) were preserved or increased in 2 of the 3 subjects in whom mouth occlusion pressure (P0.1) was augmented in the immediate (second breath) response to the load. In the third subject who showed no change in P0.1, VE was not preserved during loading. During NREM sleep, the loading response was highly consistent in all trials and in all 3 subjects. P0.1 on the second loaded breath was not increased; thus VE, VT and VT/TI were reduced over five loaded breaths. This absence of immediate load compensation during NREM sleep was similar during normoxia, hyperoxia, and hypercapnia. During sustained loading in NREM sleep VE and VT returned toward control levels coincident with an increase in end tidal CO2. We conclude that augmentation of inspiratory neural drive sufficient for immediate compensation to elastic loads requires wakefulness. Compensatory responses to loading do not occur during NREM sleep until inspiratory effort is augmented by chemical stimuli.
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PMID:Effects of slow wave sleep on ventilatory compensation to inspiratory elastic loading. 670 80

In the unanesthetized dogfish, Scyliorhinus canicula, oxygen and carbon dioxide partial pressures and concentrations in inspired and expired water and the acid-base balance of arterial blood, pHa and PcCO2, were determined. Each dogfish was exposed to waters differing in oxygenation and in CO2 levels, which was controlled with a pH-CO2-stat device, for successive 2- to 3-h periods. The four ambient conditions were: normoxia-normocapnia (inspired PO2, PIO2 ca 160 Torr; PICO2 ca 0.3 Torr), hyperoxia-normocapnia (PIO2 ca 730 Torr), hyperoxia-hypercapnia (PICO2 ca 1.0 Torr); normoxia-hypercapnia. At both low and high ambient CO2, the inspired-expired O2 and CO2 concentration differences increased in hyperoxia. Ventilation was depressed, and concomitantly, PACO2 increased and the arterial plasma pH decreased. The hypercapnic acidosis was rapidly but only partially compensated by an increase of the plasma bicarbonate concentration. Due to the buffer action of carbonate in sea water, low and high ambient CO2 levels corresponded respectively to high and low values of the CO2 capacitance coefficient, betaWCO2. At both ambient oxygenation levels, the expired-inspired PCO2 difference was greater at low than at high betaWCO2. At a given ambient CO2 level, expired PCO2, PECO2, wash higher in hyperoxia than in normoxia; an effect more marked at low than at high betaWCO2. Thus, the water capacitance coeffcient betaWCO2 is an important factor determining PECO2 values and probably arterial blood acid-base balance. As a general conclusion, the acid-base balance of the arterial blood in the dogfish is very much dependent on the conditions of the oxygenation and acid-base balance of the ambient water which consequently should be carefully controlled.
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PMID:Blood acid-base balance as a function of water oxygenation: a study at two different ambient CO2 levels in the dogfish, Scyliorhinus canicula. 677 56

Survival time in conditions of hyperbaric oxygenation were measured in trout and eels in water, and in frog in water or in gas phase at various temperatures. In eel and trout, the gill surface is altered within 90 min at 15 ata pressure of oxygen. Survival times of the frog during hyperoxia in aquatic or gaseous conditions are only slightly different, in spite of the marked difference in the oxygen concentration of the two media. Oxygen toxicity is well correlated with the aerobic metabolic rate, (1) in a given species adapted to various temperatures; (2) in trout eel and frog observed at the same temperature. The differing O2 toxicities in homeothermic and poikilothermic animals are also related to the differences in metabolic activity.
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PMID:A comparative study of oxygen toxicity in vertebrates. 697 78

Gill ventilation frequency (fG), the pressure amplitude (PBC) and stroke volume (VS) of buccal ventilation cycles, the frequency of air breaths (fL), water flow over the gills (VW), gill oxygen uptake (MGO2), oxygen utilization (U), and heart frequency (fH) have been measured in unanaesthetized, air breathing Rana catesbeiana tadpoles (stage XVI-XIX). The animals were unrestrained except for ECG leads or cannulae, and were able to surface voluntarily for air breathing. They were subjected to aquatic normoxia, hyperoxia and three levels of aquatic hypoxia, and their respiratory responses recorded in the steady state. The experiments were performed at 20 +/- 0.5 degrees C. In hyperoxia there was an absence of air breathing, and fG, PBC and VW fell from the normoxic values, while U increased, resulting in no significant change in MGO2. Animals in normoxia showed a very low fL which increased in progressively more hypoxic states. VW increased from the normoxic value in mild hypoxia (PO2 = 96 +/- 2 mm Hg), but fell, associated with a reduction in PBC, in moderate (PO2 = 41 +/- 1 mm Hg) and severe (PO2 = 21 +/- 3 mm Hg) hypoxia in the presence of lung ventilation. Gill MGO2 was not significantly different from the normoxic value in mild hypoxia but fell in moderate hypoxia, while in severe hypoxia oxygen was lost to the ventilating water from the blood perfusing the gills. There was no significant change in fH from the normoxic value in either hypoxia or hyperoxia. These data indicate, that in the bimodally breathing bullfrog tadpole, aquatic PO2 exerts a strong control over both gill and lung ventilation. Furthermore, there is an interaction between gill and lung ventilation such that the onset of a high frequency of lung ventilation in moderate and severe hypoxia promotes a suppression of gill ventilation cycles.
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PMID:Gill and lung ventilation responses to steady-state aquatic hypoxia and hyperoxia in the bullfrog tadpole. 697 6

To assess the effects of muscle relaxation on the critically ill ventilated neonate, pancuronium bromide was administered for a 12-hour period to ten low-birth-weight neonates (960 to 2,000 gm) of 26 to 34 weeks gestation, all whom required mechanical ventilation and were studied within 48 hours of birth (six to 39 hours). The infants were also studied for a 12-hour period during which no pancuronium bromide was administered. During both study periods, the order of which was randomized, heart rate, blood pressure, PO2, and intracranial pressure were continuously measured. The amounts of handling during the pancuronium and control periods were similar. The results revealed a significantly greater duration of hypoxia (PO2 less than 50 torr) (56.1 vs 23.6 minutes, P less than .001) and hyperoxia (PO2 greater than 70 torr) during the control period (92.5 vs 13 minutes, P less than .001). Durations of intracranial pressure elevation 10 cm H2O above the infant's baseline were significantly less during paralysis (6.7 vs 58.8 minutes, P less than .001) as were spikes of intracranial pressure to greater than 25 cm H2O (1.6 vs 24.4, P less than .05). There was no significant improvement in blood gas values, fractional inspiratory oxygen, or ventilator settings during muscle relaxation. Pancuronium reduced periods of nonoptimal oxygenation and elevated intracranial pressure and may therefore help to decrease adverse sequelae for the low-birth-weight, ventilated neonate.
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PMID:Controlled evaluation of muscle relaxation in the ventilated neonate. 701 40

To determine the effects of high oxygen (O2) tension on pulmonary vascular reactivity, we exposed rats either to 100% O2 for 48 hours or 40% O2 for 3 to 5 weeks. Lungs from all rats were isolated, blood perfused and ventilated, and pressor responses to airway hypoxia and to infused angiotensin II were measured. We found that chronic subtoxic hyperoxia did not augment subsequent hypoxic vasoconstriction, and that 48 hrs of 100% O2 markedly blunted hypoxic vasoconstriction. Meclofenamate restored hypoxic vasoconstriction to control levels in the lungs with blunted responses. Evidence for O2 toxicity in the lungs exposed to 100% O2 included interstitial swelling with alveolar exudates seen by light microscopy, and lung edema by water content calculations. We conclude that 1) chronic subtoxic hyperoxia does not influence subsequent hypoxic vasoconstriction, and 2) a dilator prostaglandin produced in the lung is a potent inhibitor of hypoxic vasoconstriction in O2 toxic lungs.
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PMID:Blunted pulmonary pressor responses to hypoxia in blood perfused, ventilated lungs isolated from oxygen toxic rats: possible role of prostaglandins. 729 93

Experiments were performed to determine the influence of varying inspired oxygen tension on renal prostaglandin E2 (PGE2) excretion, renal hemodynamics, and water and electrolyte excretion in the conscious dog. Hypoxic exposure (PIO2 = 56 torr) resulted in a 13% increase in renal blood flow (RBF), while hyperoxic breathing with PIO2 of 700, 1426, or 2139 torr, all resulted in significant 5--7% decline in RBF, a response that was significantly attenuated compared to the striking renal vasoconstriction caused by hyperoxia in anesthetized dogs. Hyperbaric oxygenation (HBO) (1426 torr O2, 2139 torr O2) was associated with unexpected decreases in urine flow (V) of 61% and 70%, respectively. The antidiuresis and mild hemodynamic adjustments were correlated with a 67% decline in urinary PGE2 excretion (UPGE2 x V) when the dogs breathed 700 torr O2, while exposure to 1426 torr O2 and 2139 torr O2 diminished UPGE2 x V by 92% and 99%, respectively. Plasma antidiuretic hormone (ADH) concentration, measured during exposure to 1426 torr O2, was unchanged. In addition, this nonpharmacologic hyperbaric decline in PGE2 excretion was not associated with any changes in sodium excretion of renin secretion, in contrast to the usual depression of these variables with pharmacologic PG inhibition (indomethacin). The HBO antidiuresis may be a consequence of an increased medullary osmotic gradient secondary to reduced vasa recta blood flow. Alternatively, this antiduresis could occur as a consequence of a lowering of the normal functional antagonism existing between PGE2 and ADH, such that the influence of endogenous ADH is potentiated.
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PMID:Antidiuresis and inhibition of PGE2 excretion by hyperoxia in the conscious dog. 740 49

In full-term newborn rats, propylthiouracil (PTU) treatment has been previously shown to decrease susceptibility to O2-induced lung damage and improve survival during hyperoxic exposure. However, no differences were found in lung antioxidant enzyme (AOE) activity responses to hyperoxia compared with O2-exposed untreated (control) term rats. To further explore possible pulmonary protective effects of PTU treatment in prematurely delivered animals, we administered PTU (0.015%) in drinking water to timed-pregnant rats for the final 10 d of gestation prior to delivery 1 d before term, and during lactation; control pregnant/nursing rats received untreated water. Both groups of 21-d premature rat pups were randomized to either > 95% O2 or room air exposure after birth for up to 14 d. The left lungs of 7-d exposure pups were used to quantitate the concentrations of AOE mRNA by solution hybridization; the right lungs of the same pups were assayed for AOE activities. PTU treatment resulted in survival rates of O2-exposed preterm rat pups that were consistently higher at all time periods in hyperoxia including 7 d [PTU, 67 of 82 (82%) versus control pups, 58 of 113 (51%); p < 0.001] and 14 d [PTU, 31 of 39 (79%) versus control, 15 of 66 (23%); p < 0.001]. Further evidence of increased tolerance to > 95% O2 in PTU pups included a significant decrease in the incidence of microscopic intraalveolar edema and a significant increase in lung tissue surfactant-related phospholipids compared with O2-exposed control pups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Premature rats treated with propylthiouracil show enhanced pulmonary antioxidant enzyme gene expression and improved survival during prolonged exposure to hyperoxia. 749 49


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