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

High hydrostatic pressure has been shown to reverse the anesthetic effects of barbiturates. However, attempts to distinguish between two possible causes of this reversal, changes in drug disposition or changes in drug-receptor interaction, have not been reported. This study examined the possible effects of hyperbaria and hyperbaric hyperoxia on the distribution and clearance of pentobarbital in the dog. The drug was administered to six mixed-breed dogs as a 30 mg/kg i.v. bolus at 1 ATA breathing air, 6 ATA breathing air, and 2.8 ATA breathing 100% oxygen, with serial blood sampling for 12 h. Pharmacokinetic and statistical analyses showed no significant effects of hyperbaria or hyperbaric hyperoxia on the total plasma clearance, volume of distribution or elimination half-life. If pressure reversal of barbiturate anesthesia occurs at these pressures, changes in the disposition of the drug are not the causative factors.
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PMID:Pharmacokinetics of pentobarbital under hyperbaric and hyperbaric hyperoxic conditions in the dog. 665 25

The influence of the depth of anaesthesia on the contribution of central and peripheral chemoreceptors to the slope of the ventilatory response to CO2 during hyperoxia was studied in 12 cats anaesthetized with chloralose-urethane or pentobarbital. By artificial perfusion of the pontomedullary region of the brainstem it was possible to assess the peripheral (Sp) and central (Sc) ventilatory sensitivity to CO2, as well as to vary selectively the level of anaesthesia at the ponto-medullary region (central level) or the overall level. In each cat Sp and Sc were assessed at the initial and at one or two deeper anaesthetic levels. Going from the initial to deeper anaesthetic levels both Sp and Sc decreased. However, Sp/Sc did not change significantly, whether the overall or the central level of anaesthesia was increased. Also the B-value, i.e. the PaCO2 of the extrapolated ventilation-PaCO2 curve at zero ventilation, did not change significantly when going to deeper anaesthetic levels. It is concluded that the respiratory depression caused by the anaesthetics used is due to an influence on the respiratory integrating centres, central chemoreceptors, or both.
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PMID:Influence of the depth of anaesthesia on the peripheral and central ventilatory CO2 sensitivity during hyperoxia. 677 64

Halothane is known to inhibit the ventilatory responses to hypoxia and hypercapnia. In order to determine whether this inhibition was mediated by peripheral chemoreceptors, the authors measured the effect of halothane on the response of carotid body chemoreceptors to these stimuli. Cats were decerebrated under brief halothane anesthesia, paralyzed, and ventilated. Chemoreceptor activity was recorded from single- or few-fiber preparations of carotid sinus nerve, and the inspiratory drive was recorded from the whole phrenic nerve. Steady-state responses were measured at three levels of CO2 tension (19-92 mmHg) during hyperoxia, and at four levels of O2 tension (35-450 mmHg) at a fixed PaCO2. Both responses were measured before, during, and after 0.5-1.0 per cent halothane was inspired. The halothane inhalation was maintained for at least 30 min before the responses were obtained. Halothane reduced the slope of chemoreceptor response to hypercapnia to about 48 per cent of the control slope. The response to hypoxia was reduced to about 58 pr cent of the control response. The increase in firing after intravenous nicotine (100 micrograms), summed for 20 s, was reduced to 25 per cent of the prehalothane control values; that after NaCN (25 micrograms) was reduced to 17 per cent of the control value. The effect of halothane was prompt (half complete in 1-2 min) and reversible. This finding explains some of the inhibition of the ventilatory responses to hypoxia and hypercapnia caused by halothane.
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PMID:Halothane depresses the response of carotid body chemoreceptors to hypoxia and hypercapnia in the cat. 711 37

The correlation between maternal PaO2 levels and umbilical vein (UV) and umbilical artery (UA)PO2 levels was studied in 40 healthy patients undergoing elective cesarean sections under lumbar epidural anesthesia. Patients were divided into four equal groups. Each group inhaled oxygen at a FIO2 of 0.21, 0.47, 0.74 (in nitrogen), or 1.0. Maternal arterial samples and fetal UV and UA samples were collected at the time of delivery. Maternal PaO2 levels increased from 96 +/- 4 (1 SE) torr during exposure to to a FIO2 of 0.21 to 232 +/- 6, 312 +/- 16, and 423 +/- 6 torr while breathing FIO2 of 0.47, 0.74 and 1.0, respectively. UV PO2 levels increased from 28 +/- 1 to 36 +/- 1.5, 41 +/- 1.3 and 47 +/- 1.2 torr in the hyperoxic groups. UA PO2 levels increased from 15 +/- 0.7 to 19 +/- 0.8, 21 +/- 0.3, and 25 +/- 1.8 torr, respectively. Oxygen saturation and blood O2 contents increased in maternal and fetal blood. Maternal arterial, UV, and UA base excess values in the hyperoxic groups were significantly higher than in the normoxic groups. There was no difference in 1- or 5-minute Apgar scores between the normoxic and hyperoxic groups. It is concluded that maternal hyperoxia improves fetal oxygen stores and acid-base status during cesarean section under epidural anesthesia.
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PMID:Oxygen transfer from mother to fetus during cesarean section under epidural anesthesia. 720 Dec 55

The value of continuous transcutaneous oxygen (PtcO2) monitoring in the presence of halothane and nitrous oxide (N2O) was studied in 10 infants. All infants were continuously monitored during the study with a Clark-type skin electrode with Mylar membrane. The polarization voltage of the membrane was changed to 600 mV to make it insensitive to N2O and halothane. The accuracy of PtcO2 electrode was compared with simultaneously measured PaO2 at different intervals. Correlation of PaO2 with PtcO2 was sought during hypoxic-normoxic state (PaO2 between 27--92 torr) and hyperoxic state (PaO2 between 105--439 torr). During hypoxic-normoxic state, the correlation between PaO2 and PtcO2 values was 0.94. During the hyperoxic state, poor correlation existed between PaO2 and PtcO2 (r = 0.51). Although PtcO2 did not correlate with PaO2 during hyperoxia, it consistently overestimated PaO2 and thereby, provided a predictive ability by over-diagnosing hyperoxia. When combined with continuous monitoring of inspired oxygen tension to maintain normoxia, continuous monitoring of PtcO2 will reduce the frequency of PaO2 analysis and improve patient care during anesthesia.
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PMID:Transcutaneous PO2 monitoring during pediatric surgery. 728 9

Ventilator-induced lung injury in children and adults is characterized by an initial inflammatory phase. To investigate whether the inflammatory cytokine, IL-1, plays a role in this process, a rabbit model of ventilator-induced injury was created. Animals maintained under pentobarbital anesthesia were primed for injury by undergoing lung lavage with 22 mL/kg of saline and then ventilated for 8 h with either FIO2 0.21 and normal pressures or FIO2 1.0 and high ventilator pressures. The animals exposed to hyperoxia/hyperventilation demonstrated a greater increase in lung lavage neutrophil counts and a higher histological injury score, as well as a faster decline in oxygenation compared to the control animals. A third group of rabbits received 800 micrograms of recombinant IL-1 receptor antagonist after lung lavage and prior to the exposure to FIO2 1.0 and high ventilator pressures. These animals had significantly lower concentrations of albumin and elastase and lower neutrophil counts in their lungs after the 8-h ventilatory period compared to hyperoxia/hyperventilation rabbits. IL-1 blockade had no effect on the decline in dynamic compliance and oxygenation seen in saline-treated hyperoxic/hyperventilated rabbits. IL-1 is a mediator of acute inflammation due to ventilator-induced lung injury.
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PMID:Effect of IL-1 blockade on inflammatory manifestations of acute ventilator-induced lung injury in a rabbit model. 777 27

Moderate exposures to hyperoxia are becoming increasingly common in clinical medicine as advancing technology allows O2 to be more effectively delivered to nonintubated patients. The sensitivity of the lung to injury by a subchronic exposure to 60% O2 was investigated, using baboons and serial lobar biopsies. Because results obtained from different regions of the lung were compared, the alveolar architecture of different lung lobes of three controls was studied, with the use of electron microscopic morphometric analyses, to assess possible lobar differences in volume, surface, and numerical densities of cells and tissues. In animals exposed to 60% O2, the same techniques were used to assess specific tissue changes in the epithelial, interstitial, and endothelial compartments of the alveolar septa. All six lobes of the normal baboon lung were found to be identical with respect to alveolar architecture. Thus, for gases of low reactivity and given in high concentrations, such as O2, cross-comparisons between different lobes are appropriate. Exposure to 60% O2 was found to cause proliferation of alveolar type II epithelium, suggesting a low-grade, chronic epithelial injury. Animals allowed to recover for 8 wk in room air showed progressive changes in the alveolar interstitium, involving increases in both cells and matrix. Because sequential lobar resections were done, animals were exposed both to 60% O2 and to the effects of general anesthesia and thoracotomies. The exposure to 60% O2 for 2 wk in this experimental setting leads to an alveolar septal injury that includes a progressive interstitial fibrotic response.
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PMID:Progressive alveolar septal injury in primates exposed to 60% oxygen for 14 days. 781 Jun 84

Cerebral venous oxygen desaturation may occur when hyperventilation is employed during neurosurgical procedures. In this study, we examined the effect of arterial hyperoxia (PaO2 > 200 mmHg) on jugular bulb venous oxygen tension (PjvO2), saturation (SjvO2) and content (CjvO2) in 12 patients undergoing anaesthesia for neurosurgical procedures. Under stable anaesthetic conditions, the inspired oxygen fraction (FIO2) was varied to give four different levels of arterial oxygen tension (PaO2 100-200, 201-300, 301-400, and > 400 mmHg), at two levels of controlled hyperventilation (PaCO2(25) and 30 mmHg). In five patients, a transcranial Doppler probe was used to insonate the middle cerebral artery throughout the study period. Regression lines were constructed for each patient for the PjvO2, SjvO2 and the corresponding PaO2 for both levels of PaCO2 (all PjvO2-PaO2 and SjvO2-PaO2 regression lines r2 > 0.85, P < 0.0001). From these lines we calculated the PjvO2, SjvO2 and CjvO2 at PaO2 of 100, 250 and 400 mmHg, at each level of PaCO2 for each patient. At PaCO2 of 25 mmHg, hyperoxaemia increased PjvO2 (from 27.6 +/- 1.1 mmHg at PaO2 of 100 mmHg to 30.6 +/- 1.4 and 33.6 +/- 1.8 mmHg at PaO2 of 250 and 400 mmHg respectively) and SjvO2 (from 54 +/- 3% at PaO2 of 100 mmHg to 60 +/- 3 and 65 +/- 3% at PaO2 of 250 and 400 mmHg respectively, P < 0.05). Hyperoxaemia had a similar effect on SjvO2 and PjvO2 at a PaCO2 of 30 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of arterial oxygenation on cerebral venous oxygen saturation during hyperventilation. 782 46

Hyperoxia is a risk factor for retinopathy of prematurity (ROP), a blinding disease in infants. However, ROP develops in human infants without raised arterial oxygen levels, such as in cyanotic congenital heart disease. In these infants raised pCO2 may be a risk factor. We investigated the effect of inspired CO2 on oxygen induced retinopathy in the rat. 56 newborn Sprague-Dawley rats were exposed to high cyclical O2 for seven days. In a control group, 27 rats were exposed to negligible CO2 by the use of soda lime. In the high CO2 group, 29 rats were exposed to elevated CO2 by omitting soda lime from their chambers. Rats in both groups had a recovery period of three days in room air following cyclical O2 exposure. On the eleventh day all rats were sacrificed after intracardiac injections of fluorescein under deep anesthesia and the retinae were dissected and flat mounted for fluorescent microscopy. The ratio of vascularized:total retinal area was calculated using computer assisted image analysis. In the high CO2 group 62% +/- 7% SD of the retina was vascularized vs. 81% +/- 7% in low CO2 group (p < 0.001). Elevated inspired CO2 results in pronounced retardation of retinal vascular development in neonatal rats exposed to fluctuating raised oxygen.
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PMID:The effect of raised inspired carbon dioxide on developing rat retinal vasculature exposed to elevated oxygen. 784 26

Surfactant dysfunction contributes to the pathophysiology of adult respiratory distress syndrome (ARDS), and we hypothesized that surfactant treatment would improve experimental ARDS produced by continuous exposure to hyperoxia. Twelve healthy male baboons (10-15 kg) were anesthetized, paralyzed, and mechanically ventilated with 2.5 cmH2O positive end-expiratory pressure (PEEP) for 96 h. Baboons were divided into three groups: 1) the O2 group (n = 5) received 100% O2, 2) the surfactant group (n = 5) received 100% O2 and aerosolized porcine surfactant, and 3) a control group (n = 2) was ventilated at fractional concentration of inspired O2 of 0.21 for 96 h to control for effects of anesthesia and mechanical ventilation. Hemodynamic parameters were obtained every 12 h, and ventilation-perfusion (VA/Q) distribution was measured daily by multiple inert gas elimination technique. PEEP was increased once or twice daily to 10 cmH2O for 30 min to study its effects on measurements of VA/Q. At the end of experiments, lungs were obtained for biochemical analysis. Prolonged hyperoxia resulted in progressive worsening in VA/Q, hemodynamic deterioration, severe lung edema, and altered surfactant metabolism. Surfactant administration increased disaturated phosphatidylcholine in lavage fluid but did not improve lung edema or gas exchange. In the surfactant group, however, the addition of 10 cmH2O PEEP resulted in a greater degree of shunt reduction than did 2.5 cmH2O PEEP (47 vs. 31% in the O2 group, P < 0.05). We conclude that aerosolized porcine surfactant did not prevent pulmonary O2 injury in baboons, but it potentiated the shunt-reducing effect of PEEP.
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PMID:Natural surfactant and hyperoxic lung injury in primates. I. Physiology and biochemistry. 800 91


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