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

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

The effect of hypoxia upon the fetus is dependent upon not only the degree of hypoxia induced but probably also upon gestational age and the initial level of fetal oxygenation. Mild hypoxia (12% or over) causes fetal tachycardia, while a more severe insult may cause bradycardia. The effect of hypoxia upon FBM in human pregnancy is uncertain, but depending upon the severity of the hypoxia, it is likely that FBM is reduced or abolished. Hyperoxia has little effect upon the fetal heart rate or FBM in normal circumstances, but an increase in FBM occurs in the presence of fetal hypoxia. No significant change in fetal heart rate in human pregnancy occurs during hypercapnia which is, however, a potent stimulus to fetal breathing. On the other hand, hypocapnia caused by hyperventilation is associated with a decrease in FBM with no obvious change in fetal heart rate. Smoking is associated with a fetal tachycardia and a decrease in FBM. The decrease in FBM is small, the effect being maximal at 30 min after smoking with recovery by 90 min.
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PMID:The fetal response to changes in the composition of maternal inspired air in human pregnancy. 677 32

To determine the effects of electrical hypoglossal nerve and submental stimulation on upper airway collapsibility, we examined the pressure-volume (P-V) relationships during bilateral supramaximal stimulation of the distal cut hypoglossal nerve ends over a range of frequencies from zero to 100 Hz in the sealed upper airway of 10 anesthetized supine dogs. Animals were artificially ventilated with 50% O2 and maintained under relative hyperoxia and hypocapnia during the study to eliminate the ventilatory drive output. Sealed upper airway pressures were obtained during random injections of different volumes of air from zero to 50 ml with and without hypoglossal nerve stimulation, and the upper airway P-V curves were obtained. The characteristics of the P-V curves were as follows: (1) the upper airway compliance defined as the slope of the regression of P-V curves fell from 4.07 +/- 0.33 ml/cm H2O without stimulation to 3.02 +/- 0.30 ml/cm H2O with stimulation at 50 Hz and plateaued at frequencies greater than 50 Hz, and (2) the volume at a given pressure during stimulation was larger than that without stimulation. The effects of submental stimulation on upper airway collapsibility were similar to those of hypoglossal nerve stimulation. These results suggest that the increase of upper airway muscle tone by hypoglossal nerve or submental stimulation stiffens the upper airway and that increases in muscle tone expand the upper airway.
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PMID:Hypoglossal nerve stimulation affects the pressure-volume behavior of the upper airway. 784 6

Bilateral carotid occlusion (BCO) was performed in pentobarbital anesthetized adult rats neonatally treated with capsaicin (50 mg/kg, sc, CNT rats). Pressor and ventilatory responses to BCO in CNT rats were compared with those of littermate controls injected with a same volume of solvent (olive oil, 0.1 ml). Capsaicin was used in order to produce partial degeneration of unmyelinated C fibres related to baroreflexes and peripheral chemoreflexes. In control rats, BCO provoked in less than 5 s, hyperventilation, hypocapnia and hyperoxia. Systemic arterial hypertension and tachycardia developed more slowly. They were maximum at 65 s. At this time, ventilation was returned to control values. Hyperventilation results from the stimulation of the carotid chemoreceptors by stagnant asphyxia generated by the blood flow stop. Hypertension and tachycardia are provoked by an increase in the orthosympathetic outflow when carotid baroreceptors are unloaded. In a first time, chemoreceptors stimulation tends to oppose to the increase of heart rate in normal rats. In a second one, development of hypertension is autolimited by the stimulation of the aortic baroreceptors particularly effective in rats. Simultaneously the hyperoxic inhibition from aortic chemoreceptors, the central hypocapnia and the reperfusion of the carotid bodies lead to the suppression of hyperventilation. As hyperventilation decreases when hypertension develops, even in rats with vago-sympathetic section at low cervical level, the part of aortic baroreceptors effects is probably reduced except for the fibres travelling through superior laryngeal nerves. Carotid bodies reperfusion seems to predominate. Before any manipulations, CNT rats had lower heart rate and systemic blood pressure than controls. During BCO, initial hyperventilation was moderately prolonged as hypertension slowly developed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Bilateral carotid occlusion in the rat neonatally treated with capsaicin]. 800 42

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

Our objective was to gain insight into the role of the carotid chemoreceptors (CC) in the exercise hyperpnea. Humans and ponies were studied at rest and during submaximal exercise breathing room air. In healthy humans, alveolar ventilation (VA) was tightly matched to CO2 production (CO2) resulting in PaCO2 deviating during exercise less than 1-2 mm Hg from rest. In contrast, ponies' VA increased proportionately more than VCO2 during exercise resulting in a workload dependent hypocapnia. Attenuating CC activity through hyperoxia had no effect on exercise PaCO2 of humans but hyperoxia accentuated the exercise hypocapnia of ponies. Similarly, CC denervation accentuated the exercise hypocapnia of ponies. Healthy humans were also studied while external airway resistance was increased, which, while breathing room air, resulted in a workload dependent hypercapnia, and this hypercapnia was accentuated by hyperoxia. Finally, a majority of asthmatic humans studied were hypercapnic during exercise while breathing room air and the hypercapnia was accentuated by hyperoxia. We conclude that the CC do not provide a primary drive for the exercise hyperpnea but they "fine tune" VA to minimize disruptions of arterial blood gases. In healthy humans, attenuating CC activity has no effect on PaCO2 because the primary VA drive is closely matched to VCO2.
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PMID:The role of the carotid chemoreceptors in the control of breathing during exercise. 818 97

We determined whether the apneic threshold after active hyperventilation was different in rapid-eye-movement (REM) vs. non-REM (NREM) sleep. Sleeping dogs were repeatedly exposed to 35-45 s of hypoxia of varying severity (end-tidal PO2 40-60 Torr) that was abruptly terminated with 100% O2. Changes in breathing pattern after brief hypoxia were compared with those after a normoxia-to-hyperoxia transition, i.e., control conditions. In NREM sleep, hypoxic hyperventilation was consistently followed by central apnea, the duration of which was linearly related to the corresponding hypocapnia and/or increase in tidal volume (VT) during hypoxia. After hypoxia, expiratory duration averaged 3.5 x control value at -5-Torr change in end-tidal PCO2 and twofold increase in VT; mean expiratory duration was 5 x control value at -10-Torr change in end-tidal PCO2 and fourfold increase in VT. In REM sleep, central apnea of varying duration did occur on occasion after brief hypoxic hyperventilation, but there was no systematic relationship with magnitude of hypocapnia or increase in VT. Breathing pattern during or after hypoxia in REM was not related to temporal changes in either eye movement density or electroencephalogram frequency. Thus, in contrast to NREM sleep, in REM sleep ("phasic" or "tonic") a posthyperventilation apneic threshold was not present. We attribute this effect of REM to 1) a reduced VT response to hypoxia that would minimize inhibitory "memory" effect from lung stretch and 2) attenuated inhibitory response to any given magnitude of hypocapnia or increased VT. Active hyperventilation-induced apneic threshold may be "masked" by actions of nonchemoreceptor and nonmechanoreceptor inputs affecting respiratory motor output in REM sleep. These data are consistent with the relative absence of central apnea and periodic breathing in humans in REM sleep.
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PMID:Effects of rapid-eye-movement sleep on the apneic threshold in dogs. 822 21

The contribution of autonomic nerve activity to stomach tone and motility during central and arterial chemoreceptor excitation or inhibition was analyzed in urethane anesthetized, artificially ventilated rats. Systemic severe hypoxia at end-tidal O2 concentration (FETO2) 6% and systemic hypercapnia at end-tidal CO2 concentration (FETCO2) 6%, 8% and 10% applied for 1 min produced a significant depression in gastric tone and motility. Hypocapnia at 3% FETCO2 increased gastric tone and motility. Hypoxia co-activated both the sympathetic and the vagal efferent gastric nerve branches. Hypercapnia augmented only sympathetic gastric efferent nerve activity but not vagal efferent nerve activity. Hypocapnia slightly increased vagal nerve activity to the stomach. Bilateral denervation of the arterial chemoreceptors significantly attenuated the inhibitory gastric response to hypoxia. Similar attenuation of hypoxia-induced depression of gastric tone and motility was produced by bilateral gastric sympathectomy but not by vagotomy. In contrast, the inhibitory effect of severe hypercapnia and the facilitatory effect of hypocapnia upon gastric tone and motility were unaffected by arterial chemoreceptor denervation, by severance of gastric sympathetic branches or by gastric vagal denervation. Hyperoxia at 90% FETO2 had no effect on the gastric nerve activities, gastric tone or motility. It is concluded that in the rat hypoxia co-activates sympathetic and vagal efferent nerve activities to the stomach via an arterial chemoreceptor reflex, and that hypercapnia activates sympathetic gastric nerve activity via central chemoreceptors. Hypocapnia activates efferent vagal gastric nerve activity. All chemical stimuli except that of hyperoxia have a significant local effect on the gastric tone and motility.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of the central and arterial chemoreceptors in the response of gastric tone and motility to hypoxia, hypercapnia and hypocapnia in rats. 822 66

Near-infrared spectroscopy is a noninvasive bedside technique for monitoring hemoglobin saturation (HbO2%) in brain vasculature. The method linearly relates the optical signal detected from the surface of the head to HbO2%. To do so, the method relies on constant transcranial optical pathlength and light scattering as well as minimal interference by tissues overlying the brain. This study examined these premises. Optical signals from a dual-wavelength, near-infrared spectrometer were correlated with sagittal sinus HbO2% in 7 anesthetized piglets subjected to 7 different physiological conditions: normoxia, moderate and severe hypoxia, hyperoxia, hypocapnia, hypercapnic hyperoxia, and hypotension. These conditions were induced by varying the inspired O2 concentration (7-100%), ventilatory rate (5-35 breaths/min), and blood pressure (phlebotomy 20 ml/kg) to force HbO2% over a wide range (5-93%). To evaluate interference by tissues overlying the brain, correlations were repeated after the scalp and skull were rendered ischemic. Transcranial optical pathlength was measured by phase-modulated spectroscopy. Linear relationships between optical signals and sagittal sinus HbO2% were found with correlation coefficients ranging from -0.89 to -0.99 (p < 0.05) among animals; however, slope and intercept had coefficients of variability of approximately 15 and 333%, respectively. Almost identical linear expressions were observed whether scalp and skull were ischemic or perfused. Transcranial optical pathlength was constant in each animal, but ranged from 10 to 18 cm among animals. The data indicate that the assumptions underlying near infrared spectroscopy are reasonably accurate in a given animal, but that the constants for transcranial optical pathlength and light scattering are not the same in all animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Near-infrared monitoring of the cerebral circulation. 834 68


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