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

The effects of hypoxic hypoxia on high-energy phosphate metabolites and intracellular pH (pHi) in the brain of the anesthetized infant rabbit were studied in vivo using 31P nuclear magnetic resonance spectroscopy. Five 10- to 16-day-old rabbits were anesthetized with 1.5% halothane. Ventilation was controlled to maintain normocarbia. Inspired O2 fraction was adjusted to produce three states of arterial oxygenation: hyperoxia (PaO2 greater than 250 mm Hg), normoxia (PaO2 approximately 100 mm Hg), and hypoxia (PaO2 25-30 mm Hg). During hypoxia, blood pressure was kept within 20% of control values with a venous infusion of epinephrine. During hyperoxia, the phosphocreatine-to-ATP ratio was 0.86, a value that is 2-2.5 times less than that reported for adults. During normoxia, ATP decreased by 20% and Pi increased by 90% from hyperoxia values. During 60 min of hypoxia, the concentrations of high-energy phosphate metabolites did not change, but intracellular and arterial blood pH (pHa) decreased significantly. When hyperoxia was reestablished, pHi returned to normal and pHa remained low. These results suggest that during periods of hypoxemia, the normotensive infant rabbit maintains intracellular concentrations of cerebral high-energy phosphates better than has been reported for adult animals.
J Cereb Blood Flow Metab 1985 Dec
PMID:Effects of hypoxic hypoxia on cerebral phosphate metabolites and pH in the anesthetized infant rabbit. 405 24

Five different experiments were conducted to determine if estimated liver plasma flow and/or plasma volume were changed as a result of exposure to 2.8 atmospheres absolute (ATA) while breathing 100% oxygen or 6 ATA while breathing compressed air. The experiments were designed to separate the relative roles of the ambient pressure, the partial pressure of oxygen, the time of high oxygen exposure or some combination of these factors on any observed changes. We found that time was not a factor in the changes seen. Hyperbaria resulted in a decrease in estimated liver plasma flow at all pressures greater than 1 ATA. There was an apparent increase in plasma volume at 1.3 ATA and a return towards 1 ATA values at higher pressures. Hyperoxia resulted in a decrease in estimated liver plasma flow at 975 mm Hg but not at 912 mm Hg. The flow was then increased again at 2128 mm Hg. Plasma volume decreased significantly at 912 mm Hg returned to baseline (152 mm Hg) values at 975 mm Hg and then decreased again at 1054 and 2128 mm Hg PO2.
Aviat Space Environ Med 1985 Dec
PMID:Plasma volume and estimated liver plasma flow during hyperbaric and hyperoxic exposures in awake dogs. 408 76

1. The effects of changes in ventilation and/or alveolar P(CO2) on the baroreflex control of heart rate have been studied in seven experiments on six young men and women who had been trained to control tidal volume and respiratory frequency at various levels independent of alveolar P(CO2), during hyperoxia.2. Intravenous phenylephrine provoked transient rises of directly measured arterial pressure during which individual systolic pressures (P) were linearly related to the following pulse interval (I). Baroreflex sensitivity was expressed as the slope of the regression of I on P, and reflex setting (I(ref)) as I at a single reference arterial pressure (= mean P for the experiment).3. Voluntary control of breathing had little effect on heart rate and arterial pressure (baroreflex setting), but diminished reflex sensitivity.4. Hypercapnia regularly caused tachycardia at the reference pressure (i.e. baroreflex setting lowered). The response was completely or partly reproduced by change of P(A, CO2) at constant ventilation in four subjects but not in two others; in them change of ventilation at constant P(A, CO2) completely mimicked the effect of free-breathing hypercapnia.5. Values of baroreflex sensitivity were relatively scattered. Hypercapnia caused a fall in baroreflex sensitivity in three subjects whether ventilation was fixed or free to rise. After separating the effect of voluntarily controlling ventilation, ventilation per se was without effect on reflex sensitivity.6. It is concluded that hypercapnia and hyperpnoea have separate effects on the baroreflex, the relative magnitudes of which differ from one subject to another. Baroreflex setting and sensitivity vary independently in response to change of ventilation and of P(A, CO2).
J Physiol 1974 Dec
PMID:The effects of raising alveolar PCO2 and ventilation separately and together on the sensitivity and setting of the baroreceptor cardiodepressor reflex in man. 444 70

1. Foetal breathing movements, electrocortical activity, arterial pressure and heart rate were recorded continuously in chronically catheterized sheep, 97-145 days pregnant.2. With increasing gestational age there was a fall in heart rate of 0.67 beats/day and a rise in arterial pressure of 0.46 mmHg/day.3. Hypoxaemia in the foetus was induced by allowing the ewe to breathe low oxygen mixtures, 9% O(2) with 3% CO(2) in N(2). In the younger foetuses there was an initial rise in heart rate whereas in the older foetuses there was a fall. After the end of hypoxia there was a persistent tachycardia in both groups. In the older foetuses there was a rise of arterial pressure.4. Two vagotomized older foetuses showed cardiovascular responses similar to those of the younger foetuses.5. Foetal breathing movements were abolished by hypoxaemia in twenty-two of twenty-five experiments. In the three exceptional experiments there was a small rise in P(a, CO2).6. The proportion of time occupied by low voltage electrocortical activity in the foetus was reduced by hypoxaemia.7. Hypercapnia was induced by giving the ewe 4-6% CO(2) with 18% O(2) in N(2) to breathe. After an initial slight fall the foetal heart rate increased and there was a small rise in foetal arterial pressure.8. The proportion of time occupied by low voltage electrocortical activity and breathing movements was increased by hypercapnia.9. Maternal hyperoxia, induced by giving 50% O(2) in N(2), did not significantly increase foetal breathing movements unless the ewe was in labour. In labour the foetuses had lower P(a, O2) values initially and a reduced incidence of foetal breathing, both of which were increased by maternal hyperoxia.
J Physiol 1974 Dec
PMID:Foetal respiratory movements, electrocortical and cardiovascular responses to hypoxaemia and hypercapnia in sheep. 447 94

Daily resting and exercise electrocardiograms from 81 healthy subjects taking part in eight different air saturation chamber experiments at depths of 2-132 ft sea water gauge (fswg) were recorded and interpreted. Scalar and planar characteristics were measured and analyzed in addition to noting changes in rhythm. Of the measured variables, only the heart rate and QT-interval changed significantly in the majority of exposures. Heart rate decrements of 14%-23% were observed, generally with normalization after several days at depth, and in some cases a rebound immediately postexposure. The observed increase in QT-interval can be explained entirely by the bradycardia, which seems to be due to a combination of pressure, hyperoxia, and a chamber effect. Further distinction among these factors was not possible. Associated with the decrements in heart rate were asymptomatic supraventricular arrhythmias, generally AV-nodal escape rhythms or beats, in 10% of the subjects. One incident of symptomatic ventricular tachycardia was noted 20 h after surfacing during an exercise test. Otherwise, only infrequent, isolated premature ventricular beats were detected at depth, but were not more frequent than in the predive periods. These findings are consistent with the premise that exposure to hyperbaric air and other nitrogen-oxygen mixtures causes an increase in parasympathetic tone of sufficient magnitude to cause cardiac arrhythmias. That autonomic imbalance in diving activities may cause more malignant arrhythmias is discussed.
Undersea Biomed Res 1984 Dec
PMID:Cardiac arrhythmias and heart rate changes in prolonged hyperbaric air exposures. 608 26

The effects of a single intratracheal instillation of bleomycin followed by exposure to 70% oxygen for 72 h were studied in hamsters. Mortality increased markedly among hamsters exposed to 70% oxygen for 72 h after bleomycin instillation, compared with animals receiving bleomycin and breathing room air. The lethal dose required to kill 50% of the hamsters at 30 days (LD50, 30 day) for bleomycin alone was 0.73 U/100 g body weight, whereas the LD50, 30 day for bleomycin followed by 70% oxygen fell to 0.23 U/100 g body weight. Using morphometry and light microscopy, we found that the amount of diseased lung increased in hamsters given bleomycin with hyperoxia compared with that in those treated with bleomycin alone. After 0.20 U bleomycin and air, 2.8 +/- 1.6% of the lung was abnormal, but with 0.20 U bleomycin followed by 70% oxygen, 42.7 +/- 17.9% of the lung was abnormal. At bleomycin doses that produced no apparent lesions, the addition of 70% oxygen for 72 h produced focal interstitial fibrosis at 30 days. Neither mortality nor significant histologic changes were seen in hamsters treated with saline followed by exposure to 70% oxygen for 72 h. This study demonstrates that hyperoxia potentiates bleomycin damage and suggests that the use of elevated oxygen concentrations in patients being treated with bleomycin should be minimized.
Am Rev Respir Dis 1982 Dec
PMID:Potentiation of bleomycin-induced lung injury by exposure to 70% oxygen. Morphologic assessment. 618 24

We investigated the relative contribution of peripheral and central chemosensory mechanisms to ventilatory responses to metabolic alkalosis in anesthetized cats by simultaneously measuring steady-state carotid body chemosensory activity and ventilation. The effects of graded steady-state levels of metabolic alkalosis at constant levels of arterial O2 and CO2 partial pressure (PaO2 and PaCO2, respectively) were studied first. Then the responses to isocapnic hypoxia and hyperoxic hypercapnia before and after the induction of a given level of metabolic alkalosis were studied. From the relationship between the carotid chemosensory activity and ventilation, the contribution of the two chemosensory mechanisms was estimated. The depression of ventilation that could not be accounted for by a decrease in the carotid chemosensory activity is attributed to the central effect. We found that metabolic alkalosis decreased both carotid chemosensory activity and ventilation at all levels of PaO2 or PaCO2. The ventilatory effect of alkalosis increased during hypoxia due to suppression of both peripheral chemosensory input and its interaction with the central CO2-H+ drive. During hyperoxia the central effect of alkalosis was predominant, although the peripheral effect increased with hypercapnia. We conclude that acute metabolic alkalosis suppresses both peripheral and central chemosensory drives, and its ventilatory effect grows larger with decreasing PaO2.
Am J Physiol 1983 Dec
PMID:Relative peripheral and central chemosensory responses to metabolic alkalosis. 631 76

Hyperoxia stimulates alveolar macrophages (AM) to make and release a factor which increases neutrophil adherence to nylon fiber. Production of the neutrophil adherence-stimulating factory by AM exposed to hyperoxia is maximal after AM have been exposed to hyperoxia for 72 h and requires protein synthesis by intact AM. The adherence factor is heat-labile and by column chromatography elutes in a molecular-weight range of approximately 8000-18,000 daltons. The lungs of animals exposed to hyperoxia and contribute to neutrophil-mediated lung injury from hyperoxia.
Inflammation 1983 Dec
PMID:Hyperoxia stimulates alveolar macrophages to produce and release a factor which increases neutrophil adherence. 636 Aug 88

We injected Escherichia coli endotoxin, 2.5 mg/kg, intraperitoneally in rats, sequentially quantified alveolar inflammation during a 6-day period by several techniques, and observed the effect of previous exposure to hyperoxia on the intensity of alveolitis in this model. As noted in other models of endotoxemia, we found intravascular sequestration of leukocytes and an increase in the retention of 125I albumin in the lung 4 to 6 h after the injection of endotoxin. Bronchoalveolar lavage fluid (BALF) obtained at this time only slightly stimulated the migration of neutrophils in vitro, and the numbers and types of cells recovered by lavage were normal. Fifteen h after the injection of endotoxin, however, bronchoalveolar lavage fluid stimulated both random and directed migration of neutrophils in vitro, although recovery of neutrophils by lavage was increased only slightly. By 24 h, 125I albumin retention had returned to normal levels, but the chemotactic activity of BALF remained high, and the percentage and absolute number of neutrophils recovered by lung lavage were increased markedly. The recovery of neutrophils remained significantly elevated for 3 days but declined to control levels by 6 days, whereas the recovery of alveolar macrophages was increased at this time. Exposure to 100% O2 for 36 h prior to endotoxemia accelerated and intensified neutrophil influx into the lung and increased the stimulatory effect of BALF on neutrophil migration in vitro. We conclude that a single episode of endotoxemia in the rat causes a multi-phasic alveolar inflammatory response, and that this response is accelerated and intensified by prior, mild exposure to hyperoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
Am Rev Respir Dis 1984 Dec
PMID:Neutrophil alveolitis following endotoxemia. Enhancement by previous exposure to hyperoxia. 639 7

To determine the importance of dopamine and noradrenaline as neurotransmitters during chemoreception in the cat carotid body we investigated the contents of both compounds as well as the activity of dopamine-beta-hydroxylase (DBH) under different arterial PO2 and PCO2 conditions. The superior cervical ganglion was used as a control organ. In the carotid body and the ganglion an inverse relationship exists between the catecholamine content and the DBH activity. The carotid body has a high catecholamine content with a low DBH activity whereas the superior cervical ganglion has a low catecholamine content and high DBH activity. Hypercapnia did not produce any significant change in the catecholamine content or in the DBH content of the carotid body. However, in comparison with hyperoxia, hypoxia produced a significant change (p less than 0.05) in the noradrenaline content without changing the DBH activity. The dopamine content under these conditions did not change significantly. The results may indicate that the high catecholamine content of the carotid body is the result of a high retention and/or low rate of degradation rather than of a high rate of synthesis.
J Neurochem 1983 Dec
PMID:Dopamine-beta-hydroxylase activity of the cat carotid body under different arterial O2 and CO2 conditions. 641 72


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