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

Changes in the electroencephalogram (EEG), mean arterial blood pressure (MABP), and hemoglobin saturation in brain vasculature of lightly anesthetized normothermic humans undergoing induced circulatory arrest for implantation of an automatic internal cardioverting defibrillator were studied. EEG was measured using a four-channel bipolar montage and hemoglobin saturation was measured transcranially using reflectance spectroscopy at 760 nm with an isosbestic reference at 800 nm. Hemoglobin saturation of blood in the quadriceps muscle was also measured. Thirty-two episodes of hypotension due to ventricular fibrillation were studied along with 31 episodes of hypotension related to ventricular tachycardia and rapid ventricular pacing. In a typical fibrillatory event there was a decrease in MABP followed almost immediately by changes in hemoglobin saturation of blood in the brain vasculature. The first changes in EEG were detected an average of 6.5 s (P less than 0.001, paired t test) after the beginning of change of brain vascular hemoglobin. In some cases changes in hemoglobin saturation could be detected without changes in EEG. Desaturation curves from muscle and brain were significantly different, suggesting that the brain probe was measuring hemoglobin change in a rapidly metabolizing volume of tissue that was dissimilar to the skin, muscle, and bone monitored by the probe over the quadriceps muscle. Examination of the 32 episodes of circulatory arrest revealed a marked response that began immediately with recirculation characterized by an increase of the hemoglobin saturation signal from brain vasculature to above baseline as the duration of circulatory arrest exceeded 37 s, this response is termed reperfusion hyperoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reperfusion hyperoxia in brain after circulatory arrest in humans. 236 Jul 22

Pulmonary diffusing capacities (DL) of NO and CO were determined simultaneously from rebreathing equilibration kinetics in anesthetized paralyzed supine dogs (mean body wt 20 kg) after denitrogenation (replacement of N2 by Ar). During rebreathing the dogs were ventilated in closed circuit with a gas mixture containing 0.06% NO, 0.06% 13C18O, and 1% He in Ar for 15 s, with tidal volume of 0.5 liter and frequency of 60/min. The partial pressures of NO, 13C18O, 16O18O, N2, Ar, CO2, and He in the trachea were continuously analyzed by mass spectrometry. Measurements were performed at various O2 levels characterized by the mean end-expired PO2 during rebreathing (PE'O2). In control conditions ("normoxia," PE'O2 = 67 +/- 8 Torr) the following mean +/- SD values were obtained (in ml.min-1.Torr-1): DLNO = 52.4 +/- 11.0 and DLCO = 15.4 +/- 2.9. In hypoxia (PE'O2 = 24 +/- 7 Torr) DLNO increased by 11 +/- 8% and DLCO by 19 +/- 10%, and in hyperoxia (PE'O2 = 390 +/- 26 Torr) DLNO decreased to 87 +/- 3% and DLCO to 56 +/- 8% with respect to values in normoxia. DLNO/DLCO of 3.24 +/- 0.06 (hypoxia), 3.38 +/- 0.31 (normoxia), and 5.54 +/- 1.04 (hyperoxia) were significantly higher than the NO/CO Krogh diffusion constant ratio (1.92) predicted for simple diffusion through aqueous layers. With increasing O2 uptake elicited by 2,4-dinitrophenol, DLNO and DLCO increased and DLNO/DLCO remained close to unchanged. The results suggest that the combined effects of diffusion and chemical reaction with hemoglobin limit alveolar-capillary transport of CO. If it is assumed that reaction kinetics of NO with hemoglobin (known to be extremely fast) are not rate limiting for NO uptake, the contribution of the slow chemical reaction with hemoglobin to the total CO uptake resistance (= 1/DLCO) was estimated to be 38% in hypoxia, 41% in normoxia, and 64% in hyperoxia. The various factors expected to restrict the validity of this analysis are discussed, in particular the effects of functional inhomogeneity.
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PMID:Pulmonary diffusing capacities for nitric oxide and carbon monoxide determined by rebreathing in dogs. 238 15

Acute hypocapnia decreases CBF, increases hemoglobin affinity for oxygen and causes cerebral tissue hypoxia. This tissue hypoxia is reversed with inhalation of 100% O2 in dogs. EEG slowing produced by hyperventilation is considered a manifestation of cerebral hypoxia due to decreased CBF and is thought to be reversed with hyperoxia. This study evaluated the effects of 3 gas mixtures (16% O2, 21% O2, 100% O2) on posterior frequencies of the resting and hyperventilatory EEG in normal subjects aged 23-37. Hypocapnia was maintained to an end-tidal pCO2 of 21 mm Hg for 3 min. Respiratory measures, heart rate, saO2, minute ventilation and side effects were recorded. EEG was analyzed by visual inspection and by spectral analysis. Spectral analysis evaluated total amplitude, percentile frequencies, and peak frequencies. There were significant changes from eucapnia to hypocapnia for the group in all physiologic parameters, total amplitude by spectral analysis, and posterior frequencies by visual analysis. There were no significant differences among the gases. We conclude that the EEG changes of hyperventilation are independent of the concentration of inspired oxygen over the range studied in our subjects. Symptoms of hyperventilation are likewise independent of the inspired oxygen concentration for the range studied.
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PMID:EEG and spectral analysis in acute hyperventilation. 241 22

A pulse oximeter (Ohmeda Biox 3700) and two transcutaneous systems (Radiometer TCM3) were applied simultaneously to 18 newborn infants with respiratory insufficiency. All infants had either an umbilical catheter placed in the mid thoracic aorta or a radial artery catheter. The average monitoring time was 2 hours. Arterial blood pO2, pCO2 and pH (Radiometer ABL300), arterial sO2, HbCO and metHb (Radiometer OSM3), erythrocyte 2,3 DPG concentration, and fetal hemoglobin fraction (alkali denaturation kinetic method) were measured. Using arterial sO2 and pO2 as reference, the analytical bias of pulse oximetry (-0.5 +/- 1.0%, mean +/- 1 SD) corresponded in magnitude, when converted to pO2, to that of transcutaneous - pO2 (0.6 +/- 1.4 kPa for combined O2-CO2 electrode and -0.1 +/- 2.3 kPa for single O2 electrode). Transcutaneous pCO2 showed the smallest bias (0.3 +/- 0.3 kPa). Both pulse oximetry and transcutaneous pO2 electrodes were good as trend monitors detecting rapid changes in the infants' oxygenation status. The pulse oximeter offers certain advantages in not requiring calibration or heating. The variations in the levels of fetal hemoglobin fraction (44 to 97%), pH (7.27 to 7.49), pCO2 (3.3 to 6.8 kPa) and 2,3 diphosphoglycerate concentration (1.6 to 5.9 mmol/l) between the infants studied, resulted in a variable pO2-sO2 relation (p50 2.5 to 3.5 kPa). This presents difficulties in interpreting sO2 values in sick newborn infants, and we therefore recommend caution in using a pulse oximeter to apply strict limits for avoiding hypoxia and hyperoxia in this population.
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PMID:Pulse oximetry versus transcutaneous pO2 in sick newborn infants. 245 78

Recent evidence suggests that heavy exercise may lower the percentage of O2 bound to hemoglobin (%SaO2) by greater than or equal to 5% below resting values in some highly trained endurance athletes. We tested the hypothesis that pulmonary gas exchange limitations may restrict VO2max in highly trained athletes who exhibit exercise-induced hypoxemia. Twenty healthy male volunteers were divided into two groups according to their physical fitness status and the demonstration of exercise-induced reductions in %SaO2 less than or equal to 92%: 1) trained (T), mean VO2max = 56.5 ml.kg-1.min-1 (n = 13) and 2) highly trained (HT) with maximal exercise %SaO2 less than or equal to 92%, mean VO2max = 70.1 ml.kg-1.min-1 (n = 7). Subjects performed two incremental cycle ergometer exercise tests to determine VO2max at sea level under normoxic (21% O2) and mild hyperoxic conditions (26% O2). Mean %SaO2 during maximal exercise was significantly higher (P less than 0.05) during hyperoxia compared with normoxia in both the T group (94.1 vs. 96.1%) and the HT group (90.6 vs. 95.9%). Mean VO2max was significantly elevated (P less than 0.05) during hyperoxia compared with normoxia in the HT group (74.7 vs. 70.1 ml.kg-1.min-1). In contrast, in the T group, no mean difference (P less than 0.05) existed between treatments in VO2max (56.5 vs. 57.1 ml.kg-1.min-1). These data suggest that pulmonary gas exchange may contribute significantly to the limitation of VO2max in highly trained athletes who exhibit exercise-induced reductions in %SaO2 at sea level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of incomplete pulmonary gas exchange on VO2 max. 274 10

Blood oxygen balance and acid-base equilibrium were studied in 22 Chuvash patients with hereditary erythrocytosis. Despite the lack of the anomalous types of hemoglobin in the given type of erythrocytosis a number of the patients showed secondary tissue hypoxia associated with hyperoxia of the peripheral venous blood. It is shown that tissues are capable of extracting oxygen from the blood. It is assumed that the development of tissue hypoxia in the patients is determined by a fall in the rate of oxygen diffussion from the capillaries to the tissues or by blood shunting via the arteriolo-venular anastomoses because of microcirculatory disorders. The lowering of hematocrit to the level close to normal with the aid of bloodlettings makes oxygen balance return to normal and reduces tissue hypoxia.
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PMID:[Characteristics of oxygen balance and acid-base equilibrium of the blood in patients with hereditary erythrocytosis]. 294 43

The effect of intravenous norepinephrine (NE) administration on three O2-dependent parameters of cerebral oxygenation was studied in the parietal cortex of skull intact anesthetized rats. Reflectance spectrophotometry was used to measure in vivo changes in cortical hemoglobin saturation (Hb/HbO2), blood volume (BV), and cytochrome c oxidase (cyt. a,a3) oxidation-reduction state. The influence of arterial pressure of oxygen (paO2) on norepinephrine-induced changes in cortical microcirculatory O2 delivery and cyt. a,a3 redox state was tested under conditions of normoxia, hypoxia, and hyperoxia. Norepinephrine produced cyt. a,a3 redox changes which were independent of compensatory alterations in cortical blood volume and changes in systemic blood pressure at the tested physiological extremes. During normoxia, NE caused dose-dependent systemic pressure-related increases in the oxidation level of cyt. a,a3. Conversely, in hypoxia NE caused a reduction. Microcirculatory and cyt. a,a3 redox responses to low doses of NE during hyperoxia were similar to those obtained at high doses during normoxia. The kinetic pattern of changes in hemoglobin saturation, cyt. a,a3 redox state, and cortical blood volume during normoxia and hypoxia was consistent with direct alteration in oxygen delivery to the respiratory chain and possible modification of cerebral oxidative metabolism. Blood-brain barrier alterations and vascular smooth muscle resistance changes to NE under tested conditions of oxygenation are postulated to be responsible for the observed results.
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PMID:In vivo modulation of norepinephrine-induced cerebral oxygenation states by hypoxia and hyperoxia. 299 87

In summary, the pulse oximeter provides a reliable, continuous assessment of oxygenation in newborn infants. Its rapid response time and ease of use make it a practical device for use on all sick newborns. To avoid hyperoxia it should be used in conjunction with arterial blood gas measurements and we recommend a high SaO2 alarm of 92% in infants with predominantly fetal hemoglobin. Finally, it is an improved way of monitoring oxygenation in very immature infants and in infants with bronchopulmonary dysplasia.
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PMID:Pulse oximetry--an alternative to transcutaneous PO2 in sick newborns. 367 56

To test the hypothesis that increased hypoxic ventilatory responsiveness (HVR) raised maternal ventilation and arterial oxygenation during high-altitude pregnancy and related to the birth weight of the offspring, we studied 21 residents of Cerro de Pasco, Peru (4,300 m), while eight of them were 36 +/- 0 wk pregnant and 15 of them 13 +/- 0 wk postpartum. HVR was low in the nonpregnant women (mean +/- SE shape parameter A = 23 +/- 8) but increased nearly fourfold with pregnancy (A = 87 +/- 17). The increase in HVR appeared to account for the 25% rise in resting ventilation with pregnancy (delta VE observed = 2.4 +/- 0.7 l/min BTPS vs. delta VE predicted from delta HVR = 2.6 +/- 1.7 l/min BTPS, P = NS). Hyperoxia decreased ventilation in the pregnant women (P less than 0.01) to levels similar to those measured when nonpregnant. The increased ventilation of pregnancy raised arterial O2 saturation (SaO2) from 83 +/- 1 to 87 +/- 0%, and SaO2 was correlated positively with HVR in the pregnant women. The rise in SaO2 compensated for a 0.9 g/100 ml decrease in hemoglobin concentration to preserve arterial O2 content at levels present when nonpregnant. Cardiac output in the 36th wk of pregnancy did not differ significantly from values measured postpartum. The increase in HVR correlated positively with infant birth weight. An increase in HVR may be an important contributor to increased maternal ventilation with pregnancy and infant birth weight at high altitude.
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PMID:Maternal hypoxic ventilatory response, ventilation, and infant birth weight at 4,300 m. 370 Mar 16

Under the influence of isobaric hyperoxia during 1-3 hrs the hemoglobin of laboratory mice acquires higher affinity to oxygen and buffer capacity as compared to control.
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PMID:[Effect of hyperoxia on the hemoglobin of the laboratory mouse]. 378 Oct 38


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