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

We used mechanical ventilation of the fetal lungs in utero on 11 fetal lambs at 140-145 days gestation to alter fetal blood gases and thus separate the influences of PaO2 and PaCO2 on extrauterine breathing after cord clamping. The fetus was delivered either into a 40 degrees C saline bath or onto a cold table. Mechanical ventilation was stopped 2 min after delivery and the time to onset of continuous air breathing was observed. Also two fetuses were ventilated in utero 5 or more days after chronic instrumentation at 127 days gestation; in these animals the time to onset of breathing (diaphragm EMG) was recorded after stopping the ventilator and occluding the cord. We conclude: (a) hypercapnia is a stimulus to breathing even in hyperoxia and at 40 degrees C; (b) hypocapnia delays the start of extrauterine breathing in hyperoxia at 40 degrees C; (c) hypoxia inhibits breathing in the absence of hypercapnia or cold; (d) cold overrides the effects of hypocapnia in normoxia or moderate hypoxia.
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PMID:Determinants of the onset of continuous air breathing at birth. 366 76

In dogs acutely immersed in cold water (8-13 degrees C) oxygen uptake increased and rapidly reached a maximum value (CV02 Max). A few minutes after the start of immersion colonic temperature began to fall more or less rapidly depending on the dog but always in a linear fashion. Twenty min. after the start of immersion the inspired air was switched from air to a 60% O2/40% N2 gas mixture. The switch to the hyperoxia gas mixture slowed down or even stopped the fall in colonic temperature. Concomitantly a lowering of plasma lactate concentration was observed. It may be concluded that hyperoxia improves the cold tolerance of dogs exposed to a severe cold stress. This improvement may be due to a direct effect of hyperoxia on cellular metabolism. However other effects induced by hyperoxia cannot be ruled out.
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PMID:Increased tolerance to cold induced by hyperoxia in hypothermic dogs. 384 37

Brain microsome phospholipids and their acyl groups, from temperature and oxygen acclimated goldfish, were investigated. At the lower acclimation temperature (5C) the proportion of ethanolamine- to choline-glycerophosphatides (GPE/GPC) was increased, and the proportion of phosphatidal ethanolamine value decreased. A rise in the n-6/n-3 fatty acyl group also occurred in cold acclimation. Irrespective of acclimation temperature, 25 degrees C or 5 degrees C, a partial replacement of GPC by GPE occurred when the concentration of oxygen was increased; conversely the GPE/GPC ratio decreased at the hypoxic level. The plasmalogen GPE content increased as the oxygen concentration was raised. A rise in the n-6/n-3 ratio, for ethanolamine glycerophosphatides and phosphatidyl choline, occurred when the oxygen concentration was increased (hypoxia to hyperoxia). It is concluded that the lipid alterations associated with thermal acclimation are, in part, attributable to the concomitant change in oxygen concentration.
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PMID:The effects of temperature- and oxygen-acclimation on phospholipids of goldfish (Carassius auratus L.) brain microsomes. 400 Mar 92

An over two-fold decrease in the affinity of mitochondrial MAO to serotonin was found under hyperoxia, hypoxia and cold stress. At the same time serotonin deaminase and glucosamine deaminase activity was detected in the supernatant obtained after precipitation of the mitochondria. The data obtained indicate that the modification of the catalytic properties of MAO is caused both by alteration of the molecular properties of the enzyme and structural derangement of the mitochondrial membranes.
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PMID:[Possible mechanism of the change in the catalytic properties of brain monoamine oxidase in rats]. 401 57

The effect of the elimination of input via the carotid chemoreceptor on respiratory output was examined quantitatively in anesthetized, vagotomized, and paralyzed cats. The integrated phrenic nerve activity (PNA) was recorded as an indication of output of the respiratory center. Also, the elimination of the carotid chemoreflex drive was repeatedly done by a cold block of the carotid sinus nerve at various PCO2 levels during hyperoxia, normoxia, and hypoxia. The blockade induced a reduction in PNA at each PCO2 level in every PO2 group. If the highest PNA value recorded at a high PCO2 in each PO2 condition was assigned a value of 100%, the reduction of the PNA by the blockade, i.e., the respiratory effect of the carotid chemoreflex drive, would be slightly larger during normoxia (16%) than during hyperoxia (8.7%), but would be independent of PCO2. During hypoxia, this chemoreflex effect was about 40% of a low PCO2, and decreased with increments of PCO2, finally reaching about 20% of a high PCO2 level. Furthermore, the relative contribution of the carotid chemoreceptor to respiratory output, expressed as the ratio of the PNA reduction during blockade to the PNA before blockade, was inversely proportional to both PO2 and PCO2. It is concluded that the interaction of the peripheral and central chemoreceptor drive is hypoadditive at moderate and high PCO2 levels in anesthetized cats, and this interaction is emphasized by central hypoxia.
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PMID:Effect of inactivation of carotid sinus nerve by cold block on phrenic nerve activity in cats. 407 36

In anaesthetized rabbits the influence of differential vagal cold blockade on the ventilatory response to inhaled CO2 during hyperoxia was investigated. Following total inactivation, the relationship between ventilation (V) and arterial PCO2 (PaCO2) was shifted to the left and steepened slightly over a range of modest hypercapnia, but was progressively flattened as hypercapnia intensified. The latter effect, suggestive of a vagally mediated facilitation of ventilatory CO2 responsiveness, was studied further. Differential vagal cold blockade to a temperature (5-11 degrees C) which abolished the Breuer-Hering inflation reflex (end-inspiratory tracheal occlusion no longer eliciting a prolongation of expiratory duration, TE) had no effect on V either during normocapnia or at a substantial level of hypercapnia. Only with further vagal cooling to 0 degrees C did the ventilatory depression during hypercapnia emerge, largely because TE failed to shorten in response to the hypercapnic stimulus. It is concluded that the integrity of expiratory-terminating mechanisms is crucial for the manifestation of the vagally mediated facilitation of V and its CO2 responsiveness which is evident during hyperoxic hypercapnia. A possible role is suggested for lung epithelial irritant receptors or for the tonic late-expiratory activity from pulmonary stretch receptors.
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PMID:The involvement of expiratory termination in the vagally mediated facilitation of ventilatory CO2 responsiveness during hyperoxia. 678 64

Hyperoxia after 3-day exposure at 2-4 degrees C induces more obvious disturbance of metabolites in rats than each of the factors separately. Along with decreased arginase activity in the brain and liver by 23 and 32% resp., the urine content decreases as well by 36 and 37% resp. Resistance of these animals against hyperoxia is reduced. But a preliminary 45-day cold-adaptation at 2-4 degrees C leads to a considerable activation of liver arginase and to increased content of urine in brain and liver by 32 and 30%, resp. The activation of arginase--urine system preserves under hyperoxia: the cold-adapted animals prove more resistant against hyperoxia effect. The above dynamic changes seem to be one of possible unspecific biochemical mechanisms of increasing the organism resistance against effects of extreme factors.
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PMID:[Mechanisms of the effect of cold adaptation on the resistance to hyperoxia]. 717 27

1. The present study was designed to determine the effect of sleep on the tonic output to respiratory muscle and on the level of chemical respiratory stimulation required to produce rhythmic respiratory output. 2. Chronically implanted electrodes recorded expiratory (triangularis sterni) and inspiratory (diaphragm and parasternal intercostal) electromyographic (EMG) activities in three trained dogs during wakefulness and sleep. The dogs were mechanically hyperventilated via an endotracheal tube inserted into a permanent tracheostomy. During the studies, a cold block of the cervical vagus nerves was maintained to avoid the complicating effects of vagal inputs on respiratory drive and rhythm. 3. During wakefulness, steady-state hypocapnia (partial pressure of CO2, PCO2 = 30 mmHg) abolished inspiratory EMG activity, resulting in apnoea, but the expiratory muscle became tonically active. Compared to wakefulness, the level of the tonic expiratory EMG activity was decreased in non-REM (non-rapid eye movement) sleep (median decrease = 34%, P = 0.005) and was further decreased in REM sleep (median decrease = 78%, P < 0.0001). During REM sleep, the tonic expiratory EMG activity was highly variable (mean coefficient of variation = 39% compared to 7% awake, P < 0.0001) and in some periods of REM, bursts of inspiratory EMG activity and active breathing movements were observed despite the presence of hypocapnia. 4. During constant mechanical hyperventilation, progressive increases in arterial PCO2 (in hyperoxia) were produced by rebreathing. Measurement of the CO2 threshold for the onset of spontaneous breathing showed that this threshold was not different between wakefulness and non-REM sleep (mean difference = 0.1 mmHg from paired observations, 95% confidence interval for the difference = -1.0 to +1.1 mmHg, P = 0.898). 5. The results show that sleep reduces the tonic output to respiratory muscles but does not increase the CO2 threshold for the generation of rhythmic respiratory output. These observations suggest that changes in the tonic drives to the respiratory motoneurones may be a principal mechanism by which changes in sleep-wake states produce changes in respiratory output.
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PMID:Effects of sleep on the tonic drive to respiratory muscle and the threshold for rhythm generation in the dog. 801 11

This study was designed to determine whether a chemoreceptor-mediated tonic respiratory drive exists below the apneic threshold. Expiratory (triangularis sterni) and inspiratory (diaphragm and parasternal intercostal) electromyographic activities were recorded in three awake relaxed dogs breathing through an endotracheal tube inserted into a permanent tracheostomy. The cervical vagus nerves were cold blocked to avoid the complicating effects of vagal inputs on respiratory activity. During hypocapnia produced by mechanical hyperventilation, expiratory muscle activity converted from rhythmic to tonic discharge when inspiratory muscle activity and spontaneous breathing movements were abolished. In hypocapnia, changes in arterial PCO2 (in hyperoxia) were produced by changing the ventilator rate for steady-state (> 6 min) CO2 stimuli and by disconnecting the ventilator for transient CO2 stimuli. By use of either method, a CO2-mediated drive to the expiratory muscle was consistently observed during hypocapnic apnea. At a constant level of hypocapnia, inhalation of 5% O2 consistently caused the onset of spontaneous breathing; the onset of phasic inspiratory activity was associated with reciprocal inhibition of the tonic expiratory activity. However, inhalation of 10 and 15% O2 caused an inhibition of the tonic expiratory activity, even without the onset of breathing. These results suggest that the response threshold of the respiratory chemoreceptors is lower than the apneic threshold and that a chemoreceptor-mediated tonic respiratory drive persists during apnea.
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PMID:Tonic respiratory drive in the absence of rhythm generation in the conscious dog. 817 77

Underwater diving is a widely practised leisure activity. As cardiac patients may wish to participate, cardiologists should be aware of potential changes of cardiac function during diving. Multiple factors may affect haemodynamics. Firstly, changes in pressure, secondary to ventilation of a high density gas mixture which increases afterload. Hyperoxia is the principal factor which slows the heart rate, a commonly observed phenomenon. Excitability and conduction speed may be modified by the increase in hydrostatic pressure. During decompression, gaseous pulmonary embolism may increase right heart pressures and cause a paradoxical embolism may increase right heart pressures and cause a paradoxical embolism in patients with a right-to-left shunt. Immersion increases the preload. Exposure to cold also plays a role increasing afterload and slowing the heart rate. These factors may disturb cardiac function and expose cardiac patients to accidents during underwater diving.
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PMID:[Changes in cardiac function during recreational diving]. 918 Oct 36


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