Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of hyperoxia on the arousal response to airway occlusion during non-rapid eye movement (NREM) sleep was studied in six normal male subjects with a mean age (+/- SD) of 23.5 +/- 8.7 yr by testing the response to the occlusion of a face mask covering the nose and mouth. Occlusion trials while the subjects breathed room air (room air condition) were alternated with trials in which subjects breathed a mixture of room air and oxygen adjusted to maintain a sleeping baseline arterial oxygen saturation of 98% (hyperoxic condition). The time to arousal (mean +/- SEM) was significantly longer during oxygen administration (4.1 +/- 4.5 versus 28.9 +/- 4.6 s; p < 0.002). The maximal deflections in airway pressure were measured at a supraglottic location during airway occlusion to reflect the degree of inspiratory effort. The maximal airway suction pressure preceding arousal did not differ between the room air (27.4 +/- 5.4 cm H2O) and hyperoxic conditions (26.6 +/- 5.9 cm H2O). Conversely, the rate of increase in inspiratory effort (maximal pressure) during occlusion was decreased by oxygen administration. We conclude that hyperoxia prolongs the time to arousal after airway occlusion by decreasing the rate of increase in the magnitude of inspiratory efforts, but it does not change the arousal threshold.
 ...
PMID:Effect of hyperoxia on the arousal response to airway occlusion during sleep in normal subjects. 148 20

CO2 single breaths have been performed in 7 men and 7 women in conditions of normoxia (FICO2 congruent to 0.13; FIO2 congruent to 0.21; FIN2 congruent to 0.66) and of hyperoxia (FICO2 congruent to 0.13; FIO2 congruent to 0.87). Ventilatory responses of the subjects and modifications of breathing pattern in the course of the CO2 tests were also explored in the two conditions. The results (mean +/- SEM) show that, whatever the oxygenation, men and women exhibit the same ventilatory response during a CO2 test from a qualitative point of view but with a smaller intensity in women (men: 0.37 +/- 0.088 LBTPS.min-1.Torr-1; women: 0.15 +/- 0.025 LBTPS.min-1.Torr-1; p less than 0.05). Considering men and women together, CO2 tests induced an increase of minute volume VE (p less than 0.001), VT (p less than 0.01) and rate of breathing (NS) but this response is decreased in hyperoxic conditions (p less than 0.05) mainly in men (men: 0.19 +/- 0.043 LBTPS.min-1.Torr-1; women: 0.11 +/- 0.023 LBTPS.min-1.Torr-1). These results show that sensitivity to transient hypercapnia and its interaction with hyperoxia are weaker in women than in men.
 ...
PMID:CO2 chemoreflex drive of ventilation in man: effects of hyperoxia and sex differences. 212 2

Hypoxia inhibits fetal breathing movements but after birth it stimulates breathing. These differences have long been thought to involve central nervous inhibitory mechanisms. Such mechanisms might exert a tonic inhibition of fetal breathing movements at normal fetal PaO2 and the rise in PaO2 at birth might lift this inhibitory effect. To test this hypothesis 7 fetal sheep were chronically instrumented at 125-130 days for recording electrocortical activity (ECoG), and the electromyograph (EMG) activity of the diaphragm and neck muscles. Catheters were placed in a fetal carotid and a brachial artery and in the fetal trachea. For an extracorporeal membrane oxygenation system a 12 F gauge silastic catheter was placed in the right atrium for draining fetal blood and a 9.6 F gauge catheter was placed in a carotid artery to return oxygenated blood. Three days after operation the fetuses were connected to the extracorporeal membrane oxygenation system and fetal PaO2 was raised to 65.2 +/- 4.4 mmHg (SEM) for 6 to 19 h without changing pH or PaCO2. Neither the incidence of high voltage ECoG (48.5 +/- SEM 2.0% vs 52.8 +/- 3.3%) nor of fetal breathing movements (37.3 +/- 2.6% vs 23.8 +/- 5.9%) changed during the periods of hyperoxia. Since fetal breathing movements did not become continuous, we conclude that the lower PaO2 in the fetus compared to the neonate does not exert a tonic inhibitory influence on fetal breathing movements.
 ...
PMID:Effect of hyperoxia (PaO2 50-90 mmHg) on fetal breathing movements in the unanaesthetized fetal sheep. 212 70

Research on endotoxin protection from oxygen toxicity is presently limited to the rat model since only rats have been protected by endotoxin. This study reports that endotoxin also extends survival of adult male mice in hyperoxia (greater than 99% oxygen at 1 ATA). Initially, 4-month-old male mice were treated with Boivin-extracted E. coli endotoxin and placed in hyperoxia. Zymosan-primed mice receiving 2 or 10 micrograms endotoxin, and unprimed mice receiving 10-40 micrograms endotoxin, showed moderate protection against hyperoxia; 11/15 Boivin-treated mice survived 120 hours exposure to hyperoxia with time-of-death in hyperoxia = 126.7 +/- 4.4 hours (mean +/- SEM, n = 15). This contrasts with untreated male mice; 0/4 survived 120 hours exposure to hyperoxia with mean survival = 103.5 +/- 3.5 hours. Mice receiving 20 or 60 micrograms Westphal-extracted endotoxin were not protected nor were older female mice receiving 20 micrograms Boivin-extracted endotoxin. This study suggests that age, sex, the extraction method used to obtain endotoxin, and possibly the time of year when endotoxin is administered, are important variables in allowing endotoxin to extend survival of mice in hyperoxia.
 ...
PMID:Endotoxin extends survival of adult mice in hyperoxia. 240 1

The effects of hydroxyl radical inhibition on an experimental model of normobaric pulmonary oxygen toxicity have been studied. The metal ion chelator, desferrioxamine (which inhibits hydroxyl-radical generation) or the hydroxyl-radical scavenger, dimethylthiourea (DMTU), were administered in an attempt to block hydroxyl-radical-mediated tissue injury. Lung injury was monitored in Sprague-Dawley rats by examining lung histology and bronchoalveolar lavage and by assessing pulmonary capillary permeability using the 125I-albumin lung permeability index and the lung weight:body weight ratio. Control animals had lung permeability indices 0.183 +/- 0.005 and lung weight to body weight ratio of 4.50 +/- 0.10 (all as mean +/- SEM). With increased duration of exposure to hyperoxia, there was a progressive increase in pulmonary inflammation, with thickening of alveolar membranes and atelectasis and a progressive increase in lung permeability indices (0.434 +/- 0.088 at 24 hrs; 0.954 +/- 0.165 at 48 hrs; and 1.55 +/- 0.214 at 60 hrs); and lung weight to body weight ratio (5.28 +/- 0.11 at 24 hrs; 6.54 +/- 0.23 at 48 hrs; and 8.91 +/- 0.51 at 60 hrs). Treatment with desferrioxamine provided significant protection from lung injury after 24 hrs of hyperoxia (eg., lung permeability indices 0.250 +/- 0.018; lung weight to body weight ratio 4.68 +/- 0.14, both p less than 0.025; cf. 24-hr hyperoxia controls) but no reduction in pulmonary injury was observed after 48 and 60 hrs of hyperoxia exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Modulation of normobaric pulmonary oxygen toxicity by hydroxyl radical inhibition. 282 Jun 42

Cerebrovascular dilation over PaO2 ranging from hyperoxia to moderate hypoxia is unexplained. We hypothesize that tissue acidosis is the cause. Local cortical cerebral blood flow (LCBF), tissue hydrogen ion concentration [H+]t, and tissue PO2 (PtO2) were measured with microelectrodes in the parietal cortex of 18 rats during a 30-min steady state on 60 to 10% inspired O2 (PaO2, 300 to 40 torr) during 40% N2O analgesia. Five rats kept on 60% O2/40% N2O served as controls. In 18 rats at a PaO2 of 275 +/- 7 torr (mean +/- SEM) and PaCO2 of 35 +/- 1 torr, cerebral values were: LCBF = 129 +/- 23 (mean +/- SEM) ml.100 g-1.min-1; [H+]t = 62 +/- 6 nM; and PtO2 = 25 +/- 3 torr. As PaO2 was reduced from about 300 to 40 torr, changes in these variables in percentage of control with respect to PaO2, were described by the following equations, all at P less than 0.0001: LCBF = 85.9 + 5,572/Pao2; [H+]t = 97.15 + 1,012/PaO2; and PtO2 = 108.8 - 3,492/PaO2. Simultaneous solution of the LCBF and [H+]t equations at various PaO2 revealed a slope of 8.82%/nM. Direct correlation between LCBF in ml.100 g-1.min-1 and [H+]t in nM revealed a linear relationship defined by the equation Y = -7.472 + 1.6705X (r = 0.6426) for [H+]t between 56 and 160 nM (pH = 7.25 and 6.80) but no correlation at [H+]t values between 56 and 32 nM (pH = 7.25 to 7.50). Cerebrovascular tone is directly correlated with [H+]t during progressive, 30-min steady-state reduction in PaO2 from 350 to 40 torr.
 ...
PMID:Mechanisms of cerebrovascular O2 sensitivity from hyperoxia to moderate hypoxia in the rat. 292 Dec 94

In patients with obstructive apnea, it was hypothesized that stimulation of the ventilatory system by hypercapnia during sleep would increase pharyngeal inspiratory muscle activity and thereby increase upper airway caliber. We predicted that this increase in caliber would decrease the number of apneas and sleep time spent apneic. In contrast, suppression of the ventilatory system activity with hyperoxia was predicted to decrease both inspiratory muscle activity and pharyngeal caliber and thereby increase the number of apneas and apnea time. In all 7 patients with symptomatic obstructive sleep apnea studied, 3 with upper airway narrowing obvious during wakefulness, inhalation of 3 to 6% CO2 preferentially stimulated upper airway inspiratory muscle tonic electrical activity relative to the activity of chest wall inspiratory muscles and diminished periodic breathing. Apnea time decreased from 60 +/- 2% (mean +/- SEM) of sleep time during ambient air inhalation to 12 +/- 3% during CO2 inhalation; 50% O2 had the reverse effect on inspiratory muscle tonic electrical activity and increased apnea time to 75 +/- 5% of sleep time. We conclude that manipulation of inspiratory muscle tonic activity and alteration of the pattern of breathing by CO2 and O2 inhalation lead to significant changes in the pattern of upper airway inspiratory collapse during sleep. We speculate that physiologic variables related to the control of upper airway inspiratory muscle function are instrumental in the pathophysiology of obstructive sleep apnea.
 ...
PMID:Alteration in obstructive apnea pattern induced by changes in oxygen- and carbon-dioxide-inspired concentrations. 314 3

We used the technique of lineal analysis to study the influence of 48 h of hyperoxia on cytoplasmic organelles of pulmonary granular pneumocytes with particular reference to their lamellar bodies. We undertook this study because lamellar bodies are considered to be storage granules for pulmonary surfactant and because we had found that hyperoxia decreased [(14)C]leucine incorporation into protein of a surface-active lung fraction. We found that for lamellar bodies the percent cytoplasmic volume was 12.8+/-1.5 (mean+/-SEM) and 8.4+/-2.2, the organelle area (mum(2)) per organelle was 0.98+/-0.13 and 0.62+/-0.10 and the organelle volume (mum(2)) was 0.35+/-0.04 and 0.18+/-0.01, for air- and oxygen-exposed rats, respectively, (P=<0.05). The surface density of the lamellar body membrane was 7.05+/-0.47 and 9.36+/-0.96 (P=<0.05) for air- and oxygen-exposed rats. There were no differences in lamellar body number per cytoplasmic area or per pneumocyte between air- and oxygen-exposed rats. There were no statistical differences in these parameters between mitochondria of air- or oxygen-exposed rats. The surface density of the rough endoplasmic reticulum was the same in both groups. This study indicates that granular pneumocytes of rats exposed to hyperoxia have the same number of lamellar bodies as control rats but the lamellar bodies are smaller. This findings in consistent with the hypothesis that the hyperoxia-induced decrease in protein synthesis by lung represents at least in part a decreased synthesis of the secretory lipoprotein-pulmonary surfactant.
 ...
PMID:Hyperoxia: a stereologic ultrastructural examination of its influence on cytoplasmic components of the pulmonary granular pneumocyte. 468 81

In the subjects being prepared to neurosurgical treatment an i.v. injection of NaHCO3 (2 mEq/kg) elicited a significant increase in PCSFO2 from 69 +/- 6.4 (SEM) Torr to 75.5 +/- 3.9 (SEM) Torr. This change ws accompanied by a significant drop of PaO2 from 150.5 +/- 6.0 Torr to 138.0 +/- 5.8 Torr. Metabolic alkalosis (pH 7.54 +/- 0.02 SEM) elicited by bicarbonate administration was accompanied by arterial blood hyperoxia. Both these factors reduce the cerebral flow (CBF). We suppose that changes in the blood--CSF oxygen relationship reflect the presence of a mechanism which might protect the CNS against a decrease in CBF.
 ...
PMID:Decrease of oxygen difference between arterial blood and cerebrospinal fluid after intravenous injection of sodium bicarbonate in hyperoxic patients, anaesthetized, paralyzed and artificially ventilated. 627 42

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.
 ...
PMID:The rate and regularity of breathing movements in the normal and growth-retarded fetus. 641 69


1 2 3 4 Next >>