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

Administration of monoamine oxidase type A inhibitor clorgyline to rats before hyperoxia prevented oxygen-induced increase in diene conjugate and Shiff's base brain and plasma levels in hyperoxia. This was due to antioxidative effect of clorgyline which resulted in stabilization of blood cellular membranes. Clorgyline had a normalizing effect on extraerythrocyte hemoglobin level, total peroxidase activity and glucose-6-phosphate dehydrogenase activity in the serum.
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PMID:[Effect of clorgyline on the intensity of lipid peroxidation and on erythrocyte membrane stability in hyperoxia]. 380 52

The sensitivity of the brain to cyanide-induced histotoxic hypoxia and the protective effects of known cyanide antagonists, have been assessed in vivo by reflectance spectrophotometry. Cyanide-related changes in cytochrome a,a3 (cytochrome c oxidase) oxidation-reduction (redox) state, tissue hemoglobin saturation, and local blood volume were continuously monitored in cerebral cortex of rats. Noncumulative, dose-dependent inhibition of the in situ mitochondrial respiratory chain was evaluated directly by measuring increases in reduction levels of the terminal oxidase. These transient cytochrome a,a3 reductions were accompanied by increases in regional cerebral hemoglobin saturation and blood volume. Cytochrome redox responses were not altered either in magnitude or kinetics by hyperoxia; however, the cyanide-cytochrome dose-response curve was greatly shifted to the right by pretreatment with sodium nitrite, and the recovery rate of cytochrome a,a3 from cyanide-induced reduction was enhanced fourfold by pretreatment with sodium thiosulfate.
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PMID:Cyanide-induced cytochrome a,a3 oxidation-reduction responses in rat brain in vivo. 631 56

The oxygen-transport function of blood in hyperoxia and acute disturbances of the acid-alkali condition was studied in "oxygenator--desoxygenator" as a model. It has been established that in acidosis there occurs decreased intensity of glycolysis in erythrocytes, accumulation of 2,3 diphosphoglyceric acid which decreases affinity of hemoglobin for oxygen. It does not occur in alcalosis.
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PMID:[Oxygen transport function of the blood in acute disorders of gas metabolism and of the acid-base state]. 676 93

Arterial (PaCO2), alveolar (PACO2), mixed expired (PECO2) CO2 pressures, CO2 production (VCO2) as well as arterial O2 saturation (SaO2) were measured on 20 severely hypoxic and hypercapnic patients breathing air (A) and 100% O2 (HO). On HO, mean PaCO2 increased to 56.6 torr from 50.8 torr on A, whereas there was no significant change in PACO2 (38.3 on A, 38.6 on HO), so that the arterial-alveolar gradient (aADCO2) increased from 12.5 to 18.0 torr. PECO2 remained essentially the same. There was a statistically significant correlation between the increase in PaCO2 on HO and the arterial unsaturation (100 - SaO2) on A and also between PaCO2 on A and its increment on HO. When the rise in PaCO2 and aADCO2 were estimated which resulted from the shift in the Co2 dissociation curve due to complete oxygenation of hemoglobin on HO (Haldane effect), 78% of the observed change in PaCO2 could be accounted for. The deadspace/tidal volume ratio (VD/VT) increased from 0.59 on A to 0.64 and 87% of this difference could be attributed to the Haldane effect. The results emphasize the importance of considering this effect when interpreting alterations in PaCO2, aADCO2 and VD/VT on transition from air to hyperoxia, particularly in patients with severe hypoxemia and hypercapnia.
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PMID:Contribution of the Haldane effect to the rise of arterial Pco2 in hypoxic patients breathing oxygen. 678 Feb 65

The affinity of hemoglobin for oxygen was studied during blood incubation in oxygen, air and argon. It was shown that the affinity of hemoglobin for oxygen increased during incubation of blood and hemoglobin in oxygen and air, and remained unchanged on incubation in argon. The concentration of 2,3-diphosphoglycerin acid and glucose in blood samples drastically fell in all the experiments. A possible affinity mechanism is discussed. It is concluded that the deference reaction of the blood system to hyperoxia is triggered at the level of the hemoglobin molecule.
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PMID:[Functional properties of hemoglobin during blood incubation in oxygen]. 729 47

In 9 normal test subjects, aged 19-32, pO2, pCO2 and pH of arterial and venous blood were measured. The curve of oxyhemoglobin dissociation during 20 min inhalation of a 95% O2 containing mixture was analyzed. The studies demonstrate that during hyperoxia there is a shift to the left of the dissociation curve in native blood and standard curve (i.e. normalized to pH 7.4). This shift of the curve of oxyhemoglobin dissociation indicating an increase in hemoglobin affinity for oxygen seems to be one of the factors responsible for an increase in the pO2 arteriovenous difference and a much lower increment of venous pO2 than that of arterial pO2.
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PMID:[Effect of hyperoxia on the oxygen-transport properties of the blood]. 735 70

The limiting factor for acute anemia is myocardial oxygen supply, since arterial oxygen content is decreased by isovolemic hemodilution while myocardial oxygen demand is increased as a result of a compensatory increase of cardiac output. A theoretical model was developed which describes the relation between hematocrit, myocardial oxygen demand and the required coronary blood flow during progressive hemodilution. Using this model, the determinants of critical hematocrit and the limits of intentional acute anemia (= "permissive anemia") can be calculated based on the limits of coronary vasodilator reserve. For a normal systemic oxygen consumption of 120 ml min-1 m-2 a critical degree of hemodilution is achieved at an hematocrit of 14% and an hemoglobin content of 4.7 g dl-1, respectively. Hyperoxia with an arterial pO2 of 400 mmHg will shift the critical hematocrit to 12%. An increase of systemic oxygen consumption by a factor of three (460 ml min-1 m-2), which might be typical for a patient during the postoperative recovery phase, increases the critical hematocrit to 21%. In patients with coronary artery disease critical hematocrit levels might be much higher. We conclude that a fixed critical hematocrit as a transfusion trigger is not appropriate in most patients. Rather the indication for blood transfusions must individually appreciate the specific circumstances of the patient, such as expected blood loss and required oxygen transport capacity reserves, hemodynamic stability, coronary artery disease and systemic oxygen consumption. It is suggested that the model presented herein might be valuable for estimation of the individual critical hematocrit in a particular patient.
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PMID:[Theoretical limits of "permissive anemia"]. 757 92

Hyperoxic ventilation, used to prevent hypoxemia during potential periods of hypoventilation, has been reported to paradoxically decrease whole body oxygen consumption (VO2). Reduction in nutritive blood flow due to oxygen radical production is one possible mechanism. We investigated whether pretreatment with the sulfhydryl group donor and O2 radical scavenger N-acetylcysteine (NAC) would preserve whole body VO2 and prevent deterioration of oxygenation in gastric mucosal tissue during hyperoxia. Thirty-eight patients, requiring hemodynamic monitoring (radial and pulmonary artery catheters) due to sepsis syndrome, were included in this randomized experiment. All patients exhibited stable clinical conditions (hemodynamics, body temperature, hemoglobin, FIO2 < 0.5). A gastric tonometer was placed to measure the gastric intramucosal pH (pHi), which indirectly assesses nutritive blood flow to the mucosa. Cardiac output was determined by thermodilution and VO2 by cardiovascular Fick. After baseline measurements, patients randomly received either 150 mg.kg-1 NAC (n = 19) or placebo (n = 19) in 250 ml 5% dextrose intravenously over a period of 15 min. Measurements were repeated 30 min after starting NAC or placebo infusion, 30 min after starting hyperoxia (FIO2 = 1.0), and 60 min after resetting the original FIO2. There were no significant differences between groups in any of the measurements before treatment and after the return to baseline FIO2 at the end of the study. NAC, but not placebo infusion, caused a slight but significant increase in cardiac output and decrease in systemic vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:N-acetylcysteine preserves oxygen consumption and gastric mucosal pH during hyperoxic ventilation. 788 69

Different regimens of oxygenation were studied in rats: acute hypoxia (9,000 m, 3 hrs), acute hyperoxia (0.7 MPa O2), which caused convulsions, and their simultaneous effects. Under these conditions the following parameters were evaluated: the rate of Fe(2+)-induced chemiluminescence, content of nitrogen and peptide catabolism products (urea, urates and middle molecule peptides) as well as total peroxidase activity, content of extraerythrocyte hemoglobin and lactic acid in blood plasma. Distinct inhibition of the chemiluminescence rate was found in all the three experimental groups studied; accumulation of uric acid, middle mass peptides, extraerythrocyte hemoglobin, lactic acid as well as an increase in the total peroxidase activity were observed in hyperoxia and in simultaneous effect of hypo- and hyperoxia; total peroxidase activity was decreased in rats with acute hypoxia. Accumulation of urates and middle mass peptides was considered according to these substances capacity to inhibit free radical oxidation in vivo.
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PMID:[Chemiluminescent analysis and some indicators of nitrogen catabolism in rat blood plasma in hypoxia with subsequent hyperoxia]. 797 75

The role of the emoxipin (Em.) (2-ethyl-6-methyl-3-oxipyridine) in the correction of the free radical oxidation and allied processes in lung tissues and blood plasma under high-pressure oxygen-prolonged action has been investigated. The studied oxygen exposure (0.3 MPa, 5h) causes the lung stage of oxygen intoxication. It is confirmed by exterior morphological assessment of the lung. The lipid peroxidation increase in lung tissue and blood plasma as well as erythrocyte membranes destabilization result from oxygen exposure. Lipid peroxidation intensity was estimated by determining of content of lipid peroxidation molecular products such as diene conjugates and Shiffs' bases. Erythrocyte membranes stability was evaluated with hemoglobin yield, total iron level and total peroxidase activity in blood plasma. Emoxipin was injected intraperitoneally in a dose 150 mg per 1 kg rats' weight just before the oxygen exposure. Emoxipin is found to improve physiological state of animals and to increase their survival; it normalizes morphology of the lungs and their state; stabilizes erythrocyte membranes injured under oxygen exposure; decreases intensity of lipid peroxidation processes in the lungs and in blood plasma which was previously increased under hyperoxia.
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PMID:[Emoxipin correction of disorders of lipid peroxidation as affected by a slight excess of oxygen pressure]. 799 32


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