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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 chronic hypoxia on carotid chemoreceptor afferent activity before and after sectioning the carotid sinus nerves (CSN) were studied in cats exposed to 10% O2 for 21-49 days in a chamber at sea level. For comparison, chronically normoxic cats at sea level were also studied. The cats were anesthetized, paucifiber preparation for the measurement of carotid chemosensory activity from a small slip of CSN was made, and their steady-state responses to 4-5 levels of arterial pressure of O2 (PaO2) at a constant PaCO2 and to 3-4 levels of PaCO2 in hyperoxia were measured before and after sectioning the CSN. The chemosensory response to hypoxia in the cats with intact CSN after chronic exposure to hypoxia was not reduced relative to the cats that breathed room air at sea level. Sectioning the CSN significantly augmented the chemosensory responses to hypoxia in all the chronically hypoxic but not significantly in the normoxic cats. The responses to moderate hypercapnia during hyperoxia were not significantly changed by cutting the CSN in either group. We conclude that there is a significant CSN efferent inhibition of chemosensory activity due to chronic hypoxia in the cat. This implies that without the efferent inhibition the hypoxic chemosensitivity is increased by chronic hypoxia.
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PMID:Efferent inhibition of carotid body chemoreception in chronically hypoxic cats. 641 87

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.
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PMID:Dopamine-beta-hydroxylase activity of the cat carotid body under different arterial O2 and CO2 conditions. 641 72

It has been postulated that the respiratory acidosis associated with hyperoxia (HO) may mediate some of the metabolic effects that are traditionally attributed to the elevation in PaO2. Five subjects performed 30 min of steady-state exercise (65% VO2max) on eight occasions while inspiring either 21 or 60% O2 in combination with 0, 2, 4, or 6% CO2. Statistical significance was accepted if P less than 0.05. The four HO tests were associated with increased VO2 and lower R and blood lactate. However, when compared to the four normoxic tests, all of the hypercapnic (HC) conditions (independent of the inspired O2 percent) had statistically lower blood lactate. Hypercapnia was associated with lower R values and increased blood H+. Regression analysis demonstrated relationships between H+ and R, as well as between H+ and blood lactate. These findings are independent of whether 21 or 60% O2 was inspired, and support the hypothesis that acidosis, not PO2, mediates the effects related to HO.
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PMID:Effects of hypercapnia and hyperoxia on metabolism during exercise. 641 3

A critical review of the literature of retrolental fibroplasia indicates that the cause of this disease is not yet known. Oxygen is certainly a critical factor but it is still not possible to make precise recommendations as to the amount or the duration of therapy that is safe. We have overemphasized the role of oxygen in the past, and as a result of this the false impression has been created that RLF is a disease that can be prevented. This gross oversimplification of a complex disease with multiple causes has resulted in many unjustified malpractice claims. A study of the present epidemic indicates that excessive oxygen administration probably plays a minor role, in contrast to the first epidemic in which prolonged oxygen administration was clearly a major factor. A reasonable working hypothesis is that the developing retina is highly sensitive to any disturbance in its oxygen supply, either hyperoxemic or hypoxemic. The retinal circulation is subject to the same wide fluctuations as the cerebral circulation in newborn infants. The very low-birth-weight, sick premature infant suffers from a number of conditions, many of which can seriously disturb the retinal circulation, resulting in hypoperfusion and ischemia. These factors (immaturity, hyperoxia, hypoxia, blood transfusions, intraventricular hemorrhage, apnea, infection, hypercarbia, hypocarbia, patent ductus arteriosus, prostaglandin synthetase inhibitors, vitamin E deficiency, lactic acidosis, prenatal complications, genetic factors) may all be present in an infant. They may interact to produce various degrees of retinal damage. Nearly all of these factors cannot be prevented or controlled by our present methods of care. Unfortunately, this means that RLF is an extremely difficult disease to prevent, treat, or investigate. A disease of this complexity with multiple causes will require very large numbers of infants in any controlled study of a therapy. Retrolental fibroplasia should not be considered an avoidable iatrogenic disease in very low-birth-weight infants. Its cause in these infants is not known.
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PMID:A reexamination of the role of oxygen in retrolental fibroplasia. 641 99

The rate and regularity of fetal breathing movements (FBM) were determined in 14 women with uncomplicated singleton pregnancies, eight of whom were between 30 and 33 weeks gestation and six between 37 and 40 weeks gestation. Similar observations were made in 19 women with pregnancies complicated by severe intrauterine growth retardation, 11 of whom were between 30 and 33 weeks and eight between 37 and 40 weeks. In normal pregnancy recordings of breath-to-breath intervals showed that FBM became more regular with advancing gestational age, and the rate [breaths/min, mean (SEM)] slowed from 57.2 (1.3) at 30-33 weeks to 47.9 (0.8) at 37-40 weeks. FBM in the growth-retarded group were regular at each gestation studied and the rate was even slower than in the normal group at term, being 41.9 (1.2) at 30-33 weeks and 41.1 (1.0) at 37-40 weeks. Hyperoxia and hypercapnia appeared to have no consistent effect on fetal breathing rate. Fasting for greater than 12 h considerably reduced the rate of FBM in the normal fetus but only marginally so in those with growth retardation. It is concluded that the pattern of FBM provides more information about the fetus than the amount of time spent breathing, particularly when growth is retarded.
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PMID:The rate and regularity of breathing movements in the normal and growth-retarded fetus. 641 69

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

In Wistar rats exposed during one hour to mixtures of oxygen and carbon dioxide producing hypoxia, hypercapnia, hyperoxia and hypocapnia, and so on, adrenaline contents of the suprarenals is reduced by high concentration of carbon dioxide (30%), with or without hypoxia. Noradrenaline contents is increased by carbon dioxide (15 to 30%). Hypercapnia is more potent than hypoxia as a suprarenal stimulus.
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PMID:[CO2 and the catecholamine content of the adrenal medulla of the rat]. 644 72

In decerebrate, vagotomized, paralyzed, and ventilated cats, phrenic and respiratory-related hypoglossal discharges were evident at normocapnic normoxia or hyperoxia. Both increased progressively in hypercapnia or hypoxia. With increasing drive, onset of inspiratory hypoglossal activity began earlier relative to phrenic onset; an early expiratory hypoglossal burst was also observed. Following subanesthetic doses of chloralose, halothane, ketamine, or pentobarbital, hypoglossal activity was depressed much more than phrenic discharge. In moderate hypercapnia or hypoxia, phrenic activity increased more than hypoglossal, whereas, at high drive, the latter rose more sharply in some cats. Electromyograms of the diaphragm and genioglossus were recorded in intact awake cats to determine if their responses and those of decerebrates are comparable. Respiratory-related genioglossal discharge was evident in normocapnia. We conclude that anesthesia suppresses hypoglossal motor activities much more than those of the bulbospinal-phrenic system. Data for decerebrate cats and unanesthetized cats or humans provide no evidence of a differential distribution of chemoreceptor afferents on hypoglossal and bulbospinal-phrenic neurons, as suggested by results in anesthetized animals.
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PMID:Respiratory-related hypoglossal nerve activity: influence of anesthetics. 662 15

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

Conscious unrestrained dogs trained to breathe through a respiratory mask or, after chronic tracheostomy, through a cuffed endotracheal tube were studied in an altitude chamber operated in such a way that end-tidal PO2 was maintained at 100, 75 or 60 Torr. Each hypoxic experiment was completed within 1 h of the onset of hypoxia. At all levels of oxygenation, resting pulmonary ventilation (V), obtained from the tidal volume (VT) and ventilatory period (T), and alveolar gas tensions (PAO2, PACO2) were measured cycle-by-cycle before and during isocapnic O2-tests (IOT) at various steady levels of alveolar PCO2 ranging from 30 to 48 Torr. For this, PCO2 in the inspired gas before and during IOT was adjusted so that PACO2 remained unchanged in the course of the first few breaths which followed the switch to hyperoxia. In analysing the transient changes of V in the course IOT, it was considered that an apnoea occurred when there was no measurable deflection on the integrated pneumotachogram past a duration twice the control T from the beginning of the last recorded ventilatory cycle. (1) Control V vs. PACO2 relationships showed classic positive interaction between hypercapnia and hypoxia; (2) during IOT at PAO2 of 100, 75 or 60 Torr, an apnoea occurred, V invariably falling to zero, provided that PACO2 was below 38-35 Torr according to the level of oxygenation; (3) above that threshold PACO2 value, the residual minimum ventilation (Vres) observed during IOT was linearly related to PACO2; (4) Vres vs. PACO2 relationships showed negative interaction between hypercapnia and hypoxia. It is concluded that (a) through isocapnic O2-tests, both the peripheral and central components of the ventilatory drive can be quantitatively estimated; (b) in conscious dogs, the pulmonary ventilation appears to be entirely driven by afferent activity from the arterial chemoreceptors, even in eucapnic normoxia; (c) the lower minimum ventilation seen in the course of O2-tests from a hypoxic rather than a normoxic background is still observed at PACO2 above normal, thus cannot be due only to hypocapnia related to preceding hypoxic hyperventilation must be caused by a central respiratory inhibition directly or indirectly related to depressant effect of even moderate hypoxia.
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PMID:The ventilatory responses of conscious dogs to isocapnic oxygen tests. a method of exploring the central component of respiratory drive and its dependence on O2 and CO2. 676 43


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