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

1. Periods of breath-holding are interrupted by episodes of continuous breathing in the aquatic turtle Pelomedusa subrufa, whereas single breaths and short periods of breath-holding alternate in the terrestrial tortoise Testudo pardalis. This implies that partial pressures of O2 and CO2 in expired air are stable in Testudo in contrast to cyclic fluctuations in Pelomedusa. 2. In spite of this, air convection requirements (VA/VO2, ml BTPS/ml STPD) are not significantly different for the two species (25.4 in Testudo, 27.3 in Pelomedusa), and differences in weight-specific ventilation between the mean body weight. 3. The end-tidal PCO2 in Pelomedusa (mean 15.2 mmHg) is lower than in Testudo (mean 24.7 mmHg), which reflects aquatic CO2 elimination in Pelomedusa. 4. In Testudo, the time course of ventilation correlates with the time course of increase of end-tidal PCO2 during CO2 breathing, but no simple relationship is evident between ventilation and blood PCO2 in Pelomedusa. 5. In both species tidal volume as well as respiratory frequency increase approximately in proportion to the end-tidal PCO2, although the response to 6% CO2 breathing could be less than expected from extrapolation of the responses to 2 and 4% CO2. Both species also increase ventilation during hypoxia, but hyperoxia depresses ventilation.
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PMID:Ventilation in an aquatic and a terrestrial chelonian reptile. 62 95

Blood flow to subunits of the lung was studied in the duck by use of radioactive microspheres. In spontaneously breathing, unanesthetized animals (series I) neopulmo was slightly better perfused than the average lung and along the paleopulmonic parabronchi, blood flow was found to decrease in the direction of ventilatory gas flow and thus of decreasing PO2 and increasing PCO2 in lung gas. The effects of respiratory gases on regional lung perfusion were investigated in unidirectionally ventilated animals (series II) in which gas mixtures offered to both lungs could be controlled independently. Local hypoxia resulted in reduction of local blood flow, whereas effects from hyperoxia or CO2 could not be substantiated. Reversal of the direction of unidirectional ventilatory flow (series III), and thus reversal of the profiles of respired gas concentrations along the parabronchi, suggest that the inhomogeneity in blood flow observed in spontaneously breathing animals of series I can only in part be explained as an acute adjustment to the local hypoxia. Calculations show that this inhomogeneity of blood flow constitutes an only minor impairment of the overall gas exchange efficacy of the parabronchial lung.
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PMID:Blood flow distribution in the duck lung and its control by respiratory gases. 62 69

Resting respiratory parameters and respiratory responses to acute changes in end-tidal O2 and CO2 pressure (PETO2 and PETCO2) were investigated in Peru in 23 newborn and 4 older infants at 3.850 m and in 13 newborns at 800 m. The study was done with the subjects asleep in a thermoneutral environment. The transient increase in ventilation in both high- and low-altitude newborns was followed by a decrease in response to acute hypoxia. During hyperoxia the two groups showed a slight but not clearly significant decrease in ventilation, whereas older high-altitude infants showed a sustained decrease. All subjects showed a prompt and clear response to CO2 inhalation during hyperoxia. We conclude that ventilatory peripheral chemoreflex is not fully developed in newborns regardless of altitude. The weak link in the reflex arc may reside in the afferent component because CO2 response was not impaired. Since hypoxic response became persistent in older infants its blunting in adult high-altitude natives is not a legacy of newborns.
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PMID:Regulation of breathing in newborns at high altitude. 64 68

1. The effect on respiration of a single dose of propranolol has been studied in normal subjects. 2. The degree of beta-adrenoreceptor blockade was assessed in terms of the impaired heart-rate response to progressive exercise and the plasma propranolol concentration. 3. No effect of propranolol was demonstrated on either the ventilatory response to rebreathing CO2 in hyperoxia, or the response to progressive isocapnic hypoxia. Simple indices of maximal expiratory flow (FEV 1.0% and PEFR) were also unchanged. 4. The absence of any effect of propranolol on the chemical control of breathing in man is discussed in relation to the conflicting literature.
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PMID:Propranolol and the ventilatory response to hypoxia and hypercapnia in normal man. 72 3

In anaesthetized cats, in which the cerebrospinal fluid bicarbonate concentration was varied by a ventriculocisternal perfusion technique, the ventilatory response to CO2 during hyperoxia could be satisfactorily described by VE = S(PCSFCO2 -B). Both the slope S and the intercept B were positively and linearly related to the CSF bicarbonate concentration. Assuming that the PCSFCO2 is equal to the PCO2 in extracellular fluid, it can be shown that VE is a linear, but not a unique function of the [H+] at the site of the chemoreceptors; the slope of this relation varies with the bicarbonate concentration at that site, possibly due to chemical complex formation between HCO-3 and Ca2+ or Mg2+. Changes in the B-value were related to the location of the central chemoreceptors with the models of Pappenheimer and Berndt aand their coworkers. It was found that changes in the CSF bicarbonate concentration are reflected for 60 per cent at the site of the central chemoreceptors, and that this was independent of the cerebral perfusion. Using Berndt's model a distance between CSF and central chemoreceptors of approximately 100 micron was found; this calculated distance is relatively insensitive to relationship (logarithmic or not) between ventilation and H+ concentration and to changes in cerebral perfusion, owing to the approximate nature of the diffusion model.
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PMID:Influence of the CSF bicarbonate concentration on the ventilatory response to CO2 in relation to the location of the central chemoreceptors. 74 Nov 4

The increase in arterial-alveolar CO2 difference (D[a-A]CO2) on 100% O2 breathing was studied in healthy subjects and in chronic bronchitic patients with or without hypoxemia. This increase in D(a-A)CO2 showing the enhancement of the dead-space effect (i.e. of the ventilation/perfusion ratio; VA/Q,), resulted from increase in PaCO2 or/and from decrease in PACO2 and was only found in hypoxic bronchitic subjects. In such subjects D(a-A)CO2 increased by about 50%. This phenomenon seems to arise from the vasomotor effect of pure O2 on pulmonary circulation and the role played by the Haldane effect in increasing PaCO2 and thus D(a-A)CO2 in some subjects is very weak. In subjects where inhalation of pure O2 produced the greatest increase in D(a-A)CO2 and in VA/Q, the calculated value of the venous admixture (QSh/QT) after measurement of D(A-a)O2 at the 30th min of hyperoxia was overestimated. Indeed D(A-a) O2 was enlarged by increasing the dead-space effect under 100% O2 breathing.
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PMID:[Effects of O2 inhalation on the partial arterial-alveolar pressure of CO2 in healthy patients and in patients suffering from chronic bronchitis (author's transl)]. 91 58

An in-vitro experiment demonstrated the concentration effect of N2O (3% versus 75%) during elimination and during uptake. Other pulmonary absorption-excretion phenomena also occur simultaneously, as paired events during uptake and then during elimination:diffusion hyperoxia and diffusion anoxia; alveolar concentration of CO2, and alveolar dilution of CO2. These clinical phenomena, as well as the second gas effect, are all related, and the pulmonary absorption-excretion volume is found to depend in part on the type of ventilation:volume controlled, pressure controlled, or spontaneous respiration.
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PMID:The pulmonary absorption-excretion volume effect. 94 30

Decrease in pulmonary vascular resistance was observed in neonatal minature pigs breathing 100% O2 or 95% O2:5% CO2. The pulmonary vasodilator response to hyperoxia ventilation was reduced by indomethacin in the intact animal and in the isolated perfused lung preparation. In the isolated perfused lung preparation, it was also shown that lung alveolar pO2 rather than pulmonary arterial pO2 was responsible for the pulmonary vasodilation. The study suggests that alveolar hyperoxia induced decrease in pulmonary vascular resistance may be mediated in part by release of prostaglandins. The relevance of this study with oxygen therapy in newborn infants is also discussed.
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PMID:Modification of alveolar hyperoxia induced pulmonary vasodilatation by indomethacin. 95 69

We wanted to know wheter the paradoxical response to CO2 under various background concentrations of O2 in preterm infants was mediated at the peripheral chemoreceptors. In five preterm infants we estimated peripheral chemoreceptor activity using the immediate change in ventilation (first 30 s) when 15%, 40%, 60%, or 100% O2 was substituted for 21% O2. Potentiation between O2 and CO2 was assessed by comparing the response with and without 4% CO2. CO2 enhanced the immediate hyperventilation with hypoxia (P less than 0.005) and reduced the immediate hypoventilation with hyperoxia (P less than 0.025 for 40% O2). This effect of CO2 increased from .00% to 15% O2 (P less than 0.05). These findings suggest: 1) CO2 interacts with O2 at the peripheral chemoreceptor level, and 2) because this interaction is more pronounced with hypoxia, the flatter CO2 response we observed with hypoxia was probably not mediated through the peripheral chemoreceptors and is likely to be central in origin.
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PMID:Effects of CO2 on immediate ventilatory response to O2 in preterm infants. 99 47

The influence of hypoxic acclimatization at altitudes of 0, 5,000, or 15,000 ft on the relative susceptibility to acute oxygen poisoning was determined in 288 adult female mice. After acclimatization periods of 1, 2, 4, or 8 wk, the mice were exposed to oxygen at high pressures (OHP) of 4, 6, or 9 ATA and the times to convulsion and death recorded. A factorial analysis of variance indicated that altitude and OHP level had inverse, log-linear effects on both parameters. The duration of acclimatization progressively decreased the time to death. The onset of convulsions and death was independent of body weight. There were significant interactions on the measured parameters between various combinations of altitude, OHP level, and duration of acclimatization. While alterations in the metabolism of gamma-aminobutyric acid and high-energy compounds are common to both hypoxia and hyperoxia, the most plausible explanation of the results relates to the decrease in buffer base induced by hypoxic acclimatization which might have caused CO2 potentiation of OHP symptoms.
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PMID:Relative susceptibility of altitude-acclimatized mice to acute oxygen toxicity. 112 Jul 52


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