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

10 Blood acid-base changes were studied at 17 degrees C in immersed crabs (Carcinus maenas) exposed to hypoxic and hyperoxic conditions, by measuring the pH and the CO2 partial pressure, PbCO2, and by calculating the bicarbonate concentration. 20 Hyperoxia first induces a marked respiratory acidosis with a rise of PbCO2. This acidosis is compensated thereafter by a non-ventilatory increase of the blood buffer base concentration. These results are discussed in relation to the general problems concerning the control of the blood acid-base balance in aquatic animals.
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PMID:[Blood acid-base changes produced by variations of water oxygenation in the crab Carcinus maenas (author's transl)]. 0 15

In six healthy male volunteers at sea level (PB 747-759 Torr), we measured pH and PCO2 in cerebrospinal fluid (CSF), and in arterial and jugular bulb blood; from these data we estimated PCO2 (12) and pH for the intracranial portion of CSF. The measurements were repeated after 5 days in a hypobaric chamber (PB 447 Torr). Both lumbar and intracranial CSF were significantly more alkaline at simulated altitude than at sea level. Decrease in [HCO3-] IN lumbar CSF at altitude was similar to that in blood plasma. Both at sea level and at high altitude, PCO2 measured in the lumbar CSF was higher than that estimated for the intracranial CSF. At altitude, hyperoxia, in comparison with breathing room air, resulted in an increase in intracranial PCO2, and a decrease in the estimated pH in intracranial CSF. With hyperoxia at altitude, alveolar ventilation was significantly higher than during sea-level hyperoxia or normoxia, confirming that a degree of acclimatization had occurred. Changes in cerebral arteriovenous differences in CO2, measured in three subjects, suggest that cerebral blood flow may have been elevated after 5 days at altitude.
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PMID:Alkaline shift in lumbar and intracranial CSF in man after 5 days at high altitude. 0 73

The respiratory system is described as a feedback control system. The controller consists of the peripheral chemoreceptors and the central chemosensitive structures, the respiratory centre in the medulla oblongata and the thorax-lung pump which they drive. The controlled system is comprised of three compartments (lung, brain and the remaining tissue) connected by the blood circulation. The controlled values are arterial pH and arterial O2 partial pressure and cerebral extracellular pH. Earlier models have been improved by: (1) the dead space description, (2) the thermodynamic formulation of the CO2 dissociation equation and the simple but accurate O2 dissociation equation of the blood, (3) the alteration of the CO2 dissociation equation for the brain and the remaining tissue to accommodate recent results, (4) the application of the one-receptor-theory of central chemosensitivity, (5) the pH dependence of brain circulation, (6) the bicarbonate exchange between blood and extracellular fluid of the brain and (7) the introduction of variable circulation times. Respiratory and metabolic disturbances of the respiratory system are analyzed. The mathematical formulation of the respiratory system is a differential difference equation system. In the steady state the experimental results are reproduced fairly well. A slight discrepancy is found in the simulation of metabolic acidosis. Apparently we have assumed the sensitivity of the peripheral chemoreceptors to be too large so that the respiratory response is not correctly predicted. In the numerical solution there is an overshoot in the on-transient and a damped oscillation in the off-transient of the alveolar CO2 partial pressure during respiratory acidosis. We have varied the parameters to make deviations small. The best agreement seems to result, if the central threshold is near the normal extracellular pH of the brain. A further deviation from experimental findings is that the cerebral CO2 and H+ concentration, the blood circulation of the brain, the alveolar O2 partial tension and the ventilation show a slight oscillation in the off-transient. Except for these discrepancies the experimental results, especially the stability of the extracellular pH of the brain, are reproduced fairly well. During hypoxia there are deviations form the experimental results if the central residual activity is constant and the central threshold deviates from the normal extracellular pH of the brain. But if the central residual activity is pH dependent and if the central threshold is equal to the normal extracellular pH of the brain, then the time course of VE and the other variables agree fairly well with experimental results. There is also a good correspondence between the theoretical and experimental data during hyperoxia. During metabolic acidosis the time constant of the bicarbonate exchange between blood and extracellular fluid of the brain is important. If a time constant of one minute is assumed, then the predicted and the experimental results correspond sufficiently well.
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PMID:[Mathematical simulation of the respiratory system (author's transl)]. 1 39

Ventilation versus alveolar PCO2 relationships were determined by the steady-state method in 6 normal male subjects at rest and during positive and negative work at one load in both normoxic and hyperoxic condition. In 5 subjects the slopes of the VE-PACO2 lines during positive and negative work increased in normoxia as compared with rest. This effect was less evident in hyperoxia. It was also found that the slopes of the VE-PACO2 lines in positive and in negative work were about the same in both normoxic and hyperoxic conditions. Oxygen uptake and CO2 production during positive work is higher than during negative work. These results suggest that: 1) the disagreement between various authors on the change of the slope of the VE-PACO2 line may be due to the differences in the method of calculation of the slope or the method of the determination of VE-PACO2 lines; 2) the stimuli from the muscle spindles in the working muscle during exercise probably do not contribute to the increase in ventilatory response to CO2; 3) the increased slope of the normoxic VE-PACO2 line during exercise may be due to the interaction of several factors such as impulses from working muscles, chemosensitivity of central or peripheral chemoreceptors, adrenal-sympathetic pathways or temperature; 4) respiratory oscilations of PAO2 or PACO2 do not seem to influence the respiratory response to CO2.
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PMID:Ventilatory response to CO2 at rest and during positive and negative work in normoxia and hyperoxia. 13 51

By measuring ventilation during isocapnic progressive hypoxia, peripheral chemoreceptor sensitivity to acute hypoxia (deltaV40) was measured in five normal young men under four sets of conditions: 1) at sea level at the subject's resting PCO2, 2) at sea level with PCO2 5 Torr above resting PCO2, 3) after 24 h at a simulated altitude of 4,267 m (PB = 447 Torr) at the subject's resting PCO2 measured during acute hyperoxia, and 4) after 24 h at high altitude, with PCO2 elevated to the subject's sea-level resting PCO2. With this experimental design, we were able to systematically vary the PCO2 and [H+] at the peripheral and central chemoreceptors of man. When mean pHa was decreased from 7.424 to 7.377 without significant change in PACO2, the mean deltaV40 increased from 18.0 to 55.9 1/min. Conversely, when mean PACO2 was altered between 33.8 and 41.6 Torr with pHa held relatively constant, the mean deltaV40 did not change. This suggests that it is the H+ and not CO2 which interacts with hypoxia in stimulating the ventilation of man. An additional finding was that the intrinsic sensitivity of the peripheral chemoreceptors to acute hypoxia did not change during 24 h of acclimatization to high altitude.
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PMID:Ventilatory interaction between hypoxia and [H+] at chemoreceptors of man. 24 Jul 97

Pulmonary exchange of O2 and CO2 was measured in unidirectionally ventilated ducks in an attempt to determine lung O2 diffusing capacity, DO2. Perfusion shunt (= venous admixture) was estimated from O2 exchange in hyperoxia, and the ventilation shunt (ventilation of non-perfused parallel lung units) was estimated from exchange of the highly soluble inert gas, chloroform. Differences in the ventilation/perfusion ratio of parallel lung units were assessed from measurement of CO2 exchange using a parallel two-compartment model. DO2 values were calculated accounting for ventilation shunt, perfusion shunt, and inhomogeneity. Perfusion shunt averaged 2.7% and ventilation shunt, 9.4%. The ventilation/perfusion ratio in the two compartments differed on the average by a factor of 2.6. The uncorrected values of DO2, not accounting for lung inhomogeneities, progressively declined with increasing inspired PO2, but this dependence was less pronounced after correcting for lung inhomogeneities. The corrected value of DO2 averaged 100 mumol . min-1 . torr-1 for ducks of 1.8 kg mean body weight. DO2 did not differ when nitrogen was replaced by helium in the ventilatory gas indicating that diffusion within the air capillaries did not contribute a significant resistance to O2 uptake. The results suggest that neither functional inhomogeneities nor diffusion between lung gas and blood limit O2 uptake of the resting duck. Under conditions of elevated metabolism, however, these parameters may become rate-limiting for O2 supply.
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PMID:Gas exchange in the parabronchial lung of birds: experiments in unidirectionally ventilated ducks. 41 39

Previous studies have shown that endurance athletes are endowed with low ventilatory responses to chemical stimuli. The implications of this association have never been clear. Although recent evidence shows that exercise ventilation (VE) correlates with ventilatory chemoresponsiveness in a group of athletes, the extent to which non-athletes may differ from athletes in this regard is unknown. We have examined the relationship between ventilatory chemoresponsiveness and exercise VE in a group of 7 non-athletes, and contrasted these findings with those obtained previously from 8 endurance and 8 non-endurance athletes. Correlation lines of exercise VE with chemical responses were similar in slope and intercept for both athletes and non-athletes. However, we found that non-athletes had greater exercise VE per unit metabolic rate (VO2 or VCO2), and greater ventilatory responses to O2 and CO2, when compared with endurance athletes at equal relative work loads (P less than 0.05). The lower exercise VE/VCO2 of endurance athletes as compared with non-athletes persisted in hyperoxia, indicating that factors other than differences in hypoxic sensitivity explain the lower exercise VE of endurance athletes. Low exercise VE may be the link between low ventilatory chemosensitivity and outstanding endurance athletic performance.
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PMID:Low exercise ventilation in endurance athletes. 49 78

Using the technique of artificial ponto-medullary perfusion, the steady state ventilation during hyperoxia was measured in 15 anaesthetized cats as a function of the central PaCO2 (PaCO2) and peripheral PaCO2 (PapCO2). To a first approximation the ventilatory response was linearly related to both the central and peripheral arterial carbon dioxide pressures, viz. VE=SC . PacCO2 + Sp . PapCO2 - K where Sc and Sp represent the overall central and peripheral sensitivity to carbon dioxide. The mean ratio Sp/Sc was 0.48 (range 0.21 to 1.08). In carotid sinus denervated cats Sp was zero, while the values of Sc in these cats were in the range of Sc of cats with intact carotid sinus nerves. It is concluded that the peripse to CO2 under steady-state conditions. Chemodenervation experiments revealed that the carotid bodies play an essential role in this contribution.
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PMID:Relative contribution of central and peripheral chemoreceptors to the ventilatory response to CO2 during hyperoxia. 49 56

Cidal activities of 24-h exposures to 100% O2 and 95% O2 + 5% CO2 were assayed at 1 and 3 ATA. Studied were 21 yeasts isolated from humans: Candida albicans (8 strains), C. tropicalis (3 strains), C. krusei (3 strains), C. parapsilosis (2 strains), C. guilliermondii (2 strains), and one strain each of C. pseudotropicalis, C. stellatoidea, and Torulopsis sp. Generally, these were extremely sensitive to hyperbaric oxygen, although species and strain differences were observed. Indices of kill from 80-100 (total kill) characterized 17 of the 21 yeasts (81%). Hyperoxia (O2 +/- CO2 at 1 ATA) was not lethal. Deprivation of CO2 as a consequence of hyperbaric exposure to 100% O2 enhanced cidal activity for only 2 of 21 yeasts, whereas hyperbaric exposure to the mixture enhanced activity against four yeasts. Cidal activities were not significantly different for the remaining 15 yeasts. This response to deprivation of CO2 is different from that of bacteria, and manifests fundamental differences between procaryotic and eucaryotic cells.
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PMID:Quantitative cidal activity of hyperbaric oxygen for opportunistic yeast pathogens. 56 66

In anaesthetized rabbits the influence of vagal cold-block on the ventilatory response to lowered arterial oxygen pressure was investigated. With intact carotid chemoreflexes, lowered PaO2 caused hyperventilation, which was progressively intensified with the degree of hypoxia, regardless of whether the alveolar PCO2 was uncontrolled or kept constant at the hyperoxic control. The V-PaO2 response was to a greater extent due to an increase of respiratory rate than to one of tidal volume. During hyperoxia, vagal cold-block caused a distinct increase in ventilation provided the alveolar PCO2 was not allowed to decrease. During moderate hypoxia, vagal block caused only a slight increase in ventilation, when PACO2 was not controlled, but a distinct decrease in ventilation, when PACO2 was maintained at the hyperoxic level. Without carotid chemoreflexes, lowered PaO2 did not change ventilation at any level, provided the vagus nerves were left intact. This was due to a substantial increase in respiratory rate counteracting a corresponding decrease in tidal volume. Then vagal block led to a ventilatory depression depending on the degree of hypoxia, which was due to a simultaneous decline in respiratory rate and tidal volume. It is concluded that during hypocapnic hypoxia the vagal stretch reflex primarily inhibits the carotid chemoreflex drive of ventilation. During normocapnic hypoxia, however, the mode of interaction between the peripheral and the central chemical drive has to be considered, which without vagal feed-back is occlusive. This occlusion appears to be counteracted by a vagal mechanism sensitive to CO2 in the airways--and possibly also to a lack of O2--, mainly shortening respiratory cycle duration.
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PMID:The role of the vagus nerves in the ventilatory response to lowered PaO2 with intact and eliminated carotid chemoreflexes. 57 48


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