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

The recovery velocity of the acido-alkaline state of the intraocular fluid depended upon the ocular hemodynamics in the rabbit intraocular chamber. Oppressive action of hyperoxia and substitute hypocapnia on intraocular blood circulation was revealed. The RQ reduction described in some eye diseases and after intraocular operations can be connected with changes in gaseous composition of the intraocular fluid.
Fiziol Zh SSSR Im I M Sechenova 1986 Dec
PMID:[Role of the gas composition of intraocular fluid in the regulation of intraocular circulation]. 302 75

The purpose of this investigation was to determine the effects of breathing hyperoxic and hypoxic gas mixtures on ventilatory kinetics in the transition from submaximal exercise to rest. Eight male subjects performed three separate single blind exercise tests at 80% of their ventilatory threshold. Inspired oxygen concentration was varied in each experimental condition: test one (55% O2 -45% N2), test two (14% O2 -76% N2), and test three (21% O2 -79% N2). Ventilation, heart rate, and gas exchange were measured every 15 s for 6 min of exercise and during 9 min of recovery from exercise. Data analysis revealed no significant (p less than 0.05) differences in the kinetics of heart rate, oxygen uptake, expired volume of carbon dioxide, or ventilation among treatments during the transition from exercise to rest. Given the belief that hyperoxia attentuates the carotid bodies and hypoxia augments carotid body chemosensitivity, these findings suggest that the carotid bodies are not important regulators of VE kinetics during recovery from exercise.
Aviat Space Environ Med 1986 Dec
PMID:Effects of hypoxia and hyperoxia on ventilatory kinetics during recovery from exercise. 309 42

To further study the role of arachidonic acid metabolites in the development of hyperoxic lung injury and the function of PMNs and/or alveolar macrophages in facilitating this role, we exposed adult rabbits to greater than 95% O2 or air for 24, 40, 48, or 65 hours. At the end of each study, bronchoalveolar lavage [BAL] of the left lung was performed, and the right lung was inflated and fixed for light and electron microscopy. PGE2, 6-keto-PGF1 alpha and thromboxane B2 were measured by RIA in arterial and venous plasma at the beginning and end of each study and in BAL fluid obtained at sacrifice. Production of these three PGs by BAL cells placed in cell culture was also measured. Significant hyperoxic lung injury did not develop until 65 hours, as evidenced by significant increase in BAL total protein and percent PMNs, and by morphologic findings. At 40 hours, however, BAL fluid PGE2 and 6-keto-PGF1 alpha increased and BAL cell production of all 3 PGs was significantly increased (p less than .05). In summary, the early PG increases observed in these studies may directly contribute to the development of hyperoxic lung injury or, rather, may be representative of a generalized increase in all arachidonic acid metabolites, including the lipoxygenase pathway. The increase in BAL cell PG production and increased PG concentrations in BAL fluid prior to any increase in BAL PMNs suggest that the AM may be the source of the early arachidonic acid metabolite increase in response to hyperoxia.
Prostaglandins Leukot Med 1986 Dec
PMID:The early involvement of pulmonary prostaglandins in hyperoxic lung injury. 310 36

1. The ventilatory sensitivity to CO2 obtained from a non-steady-state step-ramp CO2 challenge (analogous to the Read rebreathing method) was compared with the one of the steady-state method. 2. Experiments were performed during normoxia on twenty cats anaesthetized with chloralose-urethane. In eight of these cats additional measurements were carried out during metabolic acidosis and alkalosis. 3. The slope of the non-steady-state ventilatory response curve to CO2 was not significantly different from the steady-state one only if the ratio of the step-wise increase in end-tidal PCO2 (PET,CO2) (A) above its resting value and the subsequent rate of rise of the PET,CO2 (R) was equal to the time constant of the central chemoreflex pathway (tau c). This also held true during metabolic acidosis and alkalosis. 4. It is predicted that in human beings during hyperoxia the ventilatory response line obtained with Read's rebreathing method is to a fair approximation shifted to the right by a value of A with respect to the steady-state response line, provided A/R = tau c. 5. We argue that Read's prescription that a PET,CO2 equilibrium should be established between mixed venous blood, arterial blood and end-tidal gas has to be regarded as an experimental condition leading to stable-experiments rather than dictated by physiological mechanisms.
J Physiol 1986 Dec
PMID:A pseudo-rebreathing technique for assessing the ventilatory response to carbon dioxide in cats. 311 73

The relationship between the activity of the buccal force pump, expressed as the time integral of positive buccal pressure, and PaO2 was investigated in conscious toads, Bufo marinus, unidirectionally ventilated at a high flow rate (240-260 ml/min). The high ventilatory flow rate meant that PaO2 was largely independent of the animal's ventilatory activity so that the relationship between pulmonary ventilation and PaO2 was effectively open-loop. The hypoxemic threshold (PaO2) for lung ventilation was 54.2 mm Hg in hypocapnia (PaCO2 = 4.7 +/- 0.3 mm Hg), 82.6 mm Hg in normocapnia (PaCO2 = 11.6 +/- 0.2 mm Hg), and 137.9 mm Hg in hypercapnia (PaCO2 = 20.1 +/- 0.1 mm Hg). Unidirectional ventilation with 20% O2 in N2, a condition in which the toads were normoxic but hypocapnic, stopped pulmonary ventilation cycles. Taken with existing evidence that hyperoxia stops pulmonary ventilation even under conditions in which PaCO2 is elevated this suggests that hypoxic and hypercapnic stimuli summate to drive lung ventilation in the toad. Bilateral denervation of the carotid labyrinths decreased pulmonary ventilation in absolute terms, but did not reduce the proportionate increase in pulmonary ventilation in response to normocapnic hypoxia, suggesting that chemoreceptors within the carotid labyrinth may contribute to, but are not solely responsible for, the hypoxemic ventilatory drive.
Respir Physiol 1987 Dec
PMID:Hypoxemic threshold for lung ventilation in the toad. 312 Feb 66

Ventilatory effects of propofol, used as a sole agent for the induction and maintenance of general anaesthesia, were studied in 14 healthy unpremedicated patients. Subarachnoid anaesthesia was established before induction of general anaesthesia. Induction was with propofol 2.5 mg kg-1 given while the patients breathed 100% oxygen. We intended to start an infusion of propofol 100 micrograms kg-1 min-1; maintain it for at least 25 min; make a first set of quasi-steady-state observations; double the infusion; and repeat observations after 25 min. The single induction bolus plus single rate infusion was not totally satisfactory: further boluses were usually needed. At induction there was apnoea in all but three patients, sometimes lasting more than 3 min; hyperventilation before induction, combined with hyperoxia, probably exaggerated this. Established ventilatory rates were generally 30% higher than awake. One patient became bradypnoeic. Tidal volume and minute ventilation, and the Tl:Ttot ratio, were reduced. Doubling the infusion rate had no clear effect on frequency or tidal volume, but it further reduced the Tl:Ttot ratio and caused an increase in PE'CO2 of 1 kPa. The ventilatory response to carbon dioxide was 58% of baseline awake control (95% confidence limits +/- 26%) at the lower infusion rate, with further slight depression when the infusion rate was doubled. Doubling the rate of infusion of propofol did not give twice the effect on ventilation, and probably is not giving twice the "depth" of anaesthesia. We cannot say if this is for pharmacokinetic or pharmacodynamic reasons.
Br J Anaesth 1987 Dec
PMID:Some ventilatory effects of propofol as sole anaesthetic agent. 312 6

An Ohmeda Biox 3700 oximeter was evaluated during treatment of 12 patients with respiratory distress. The infants were of 27-33 weeks' gestation and between 2 days and 5 months postnatal age. Blood gases were taken from indwelling arterial catheters and were measured on an ABL 30 blood gas analyser. The study tested the accuracy of the oximeter in detecting hypoxia (PaO2 less than 55 mmHg) and hyperoxia (PaO2 greater than 80 mmHg). Results are based on 175 paired observations. Guidelines are suggested for the use of the pulse oximeter under three conditions. In a newborn infant with acute respiratory distress without direct arterial access, the limits should be set at 85% (lower) and 90% (upper). In an older infant with chronic respiratory distress, the upper limit of use should be 95%. In order to avoid oxygen tensions less than 55 mmHg which would increase the risk of pulmonary vasoconstriction, however, the lower limit should be 87%. Infants with indwelling arterial lines during their first few weeks of treatment should have oxygen tension measurements and simultaneous oxygen saturation readings plotted on a graph at the bedside. The graph should be updated every 48 h to take into account changed levels of 2,3-diphosphoglycerate, haemoglobin F, and carboxyhaemoglobin and the recommended limits should be changed accordingly.
Aust Paediatr J 1988 Dec
PMID:Guidelines for the use of pulse oximetry in the non-invasive estimation of oxygen saturation in oxygen-dependent newborn infants. 314 63

Subcutaneous, transcutaneous, and conjunctival oxygen tensions (PscO2, PtcO2, and PcjO2, respectively) were measured in anesthetized dogs subjected sequentially to normoxia, hyperoxia, and hypoxia. Intravascular pressure, hemodynamic and oxygen transport variables were measured simultaneously. PtcO2 and PcjO2 closely paralleled PaO2 during normoxia, hyperoxia, and hypoxia over a wide range of arterial oxygen tensions. PtcO2 was reliable over the widest range of PaO2, with a correlation coefficient of .94. The PcjO2/PaO2 index fell at very low PaO2. The PscO2/PaO2 index decreased at both very low and very high PaO2. Only minor changes were found in hemodynamic and oxygen transport variables during hyperoxia. During hypoxia, however, cardiac output and other central hemodynamic measurements increased, while PscO2, PtcO2, and PcjO2 fell. Oxygen delivery and oxygen consumption were maintained or only slightly changed during hypoxia. All three continuous measurements of oxygen tension are reliable indices of PaO2 over a wide range under normovolemic conditions. The instruments for measuring PscO2 and PcjO2 are unheated and therefore may have advantages for human application.
Crit Care Med 1988 Dec
PMID:Continuous monitoring of tissue oxygen tension during hyperoxia and hypoxia: relation of subcutaneous, transcutaneous, and conjunctival oxygen tension to hemodynamic variables. 319 40

Buthionine sulfoximine (BSO), an inhibitor of de novo synthesis of glutathione (GSH), was used to deplete rats of GSH and determine the effect of treatment on antioxidant enzyme responses, lung injury, and the susceptibility to concurrent sublethal or lethal hyperoxia. In a preliminary experiment, total lung nonprotein sulfhydryl (NPSH) and GSH levels were measured at various times after single doses of BSO. The lowest concentrations were observed at 12 to 18 h. These experiments were used to establish a repeated dosing protocol for more prolonged GSH depletion. The lungs of rats treated with BSO for 4 days demonstrated markedly decreased GSH and NPSH levels (10 to 40% of control values) and glutathione peroxidase activity (45 to 60% of control values). Superoxide dismutase activities were elevated, glutathione reductase activity was slightly elevated, and catalase activity was unchanged. These changes were dose-responsive. The lungs of treated rats were grossly and microscopically normal. BSO treatment of additional rats did not increase susceptibility to lethal hyperoxia (greater than 98% oxygen). Combined treatment of rats with both BSO and sublethal hyperoxia (80% oxygen) for 4 days did not alter the biochemical responses demonstrated by rats treated solely with BSO. The marked increase in catalase activity obtained after hyperoxia alone was not observed in rats treated with both hyperoxia and BSO. The lungs of saline- and BSO-treated rats exposed to sublethal hyperoxia demonstrated a patchy distribution of slight perivascular and peribronchiolar edema.(ABSTRACT TRUNCATED AT 250 WORDS)
Am Rev Respir Dis 1988 Dec
PMID:The pulmonary effects of buthionine sulfoximine treatment and glutathione depletion in rats. 320 1

This study was performed to determine whether prostaglandins play a role in the increase in pulmonary blood flow in the fetal lamb caused by an increase in oxygen tension similar to that occurring at birth. To increase fetal oxygen tension without ventilating the lungs, nine pregnant ewes with chronically instrumented fetuses were exposed to 100% oxygen at 3 atmospheres absolute pressure for 20 min in a hyperbaric chamber. This exposure increased pulmonary arterial oxygen tension in the nine fetuses from 20 +/- 1 to 54 +/- 9 torr. It increased pulmonary blood flow from fetal to newborn values, 31 +/- 3 to 295 +/- 20 ml/kg/min. It did not change pulmonary arterial pressure, 52 +/- 2 torr during normoxia and 50 +/- 2 torr during hyperoxia. Treating five of these fetuses with 3.2 +/- 0.4 mg/kg of indomethacin during hyperbaric oxygenation did not alter these effects (PO2 = 51 +/- 8 torr, pulmonary blood flow = 283 +/- 13 ml/kg/min, and pulmonary arterial pressure = 48 +/- 2 torr). We conclude that the increase in pulmonary blood flow caused by an increase in oxygen tension in the fetus is not maintained by prostaglandins.
Pediatr Res 1988 Dec
PMID:Indomethacin does not diminish the pulmonary vascular response of the fetus to increased oxygen tension. 320 24


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