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

The generation of reactive oxygen species (ROS) is a steady-state cellular event in respiring cells. Their production can be grossly amplified in response to a variety of pathophysiological conditions such as inflammation, immunologic disorders, hypoxia, hyperoxia, metabolism of drug or alcohol, exposure to UV or therapeutic radiation, and deficiency in antioxidant vitamins. Uncontrolled production of ROS often leads to damage of cellular macromolecules (DNA, protein, and lipids) and other small antioxidant molecules. A number of major cellular defense mechanisms exist to neutralize and combat the damaging effects of these reactive substances. The enzymic system functions by direct or sequential removal of ROS (superoxide dismutase, catalase, and glutathione peroxidase), thereby terminating their activities. Metal binding proteins, targeted to bind iron and copper ions, ensure that these Fenton metals are cryptic. Nonenzymic defense consists of scavenging molecules that are endogenously produced (GSH, ubiquinols, uric acid) or those derived from the diet (vitamins C and E, lipoic acid, selenium, riboflavin, zinc, and the carotenoids). These antioxidant nutrients occupy distinct cellular compartments and among them, there are active recycling. For example, oxidized vitamin E (tocopheroxy radical) has been shown to be regenerated by ascorbate, GSH, lipoic acid, or ubiquinols. GSH disulfides (GSSG) can be regenerated by GSSG reductase (a riboflavin-dependent protein), and enzymic pathways have been identified for the recycling of ascorbate radical and dehydroascorbate. The electrons that are used to fuel these recycling reactions (NADH and NADPH) are ultimately derived from the oxidation of foods. Sickle cell anemia, thalassemia, and glucose-6-phosphate-dehydrogenase deficiency are all hereditary disorders with higher potential for oxidative damage due to chronic redox imbalance in red cells that often results in clinical manifestation of mild to serve hemolysis in patients with these disorders. The release of hemoglobin during hemolysis and the subsequent therapeutic transfusion in some cases lead to systemic iron overloading that further potentiates the generation of ROS. Antioxidant status in anemia will be examined, and the potential application of antioxidant treatment as an adjunct therapy under these conditions will be discussed.
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PMID:Interaction of antioxidants and their implication in genetic anemia. 1060 86

Adult, conscious rats have been exposed to CO-induced hypoxia for 30 min in normoxia, ambient hypoxia (FI(O(2))=14%), or hyperoxia (FI(O(2))=40%). From arterial blood gas analyses, FICO was adjusted in all experimental conditions to obtain final arterial oxygen saturations (Sa(O(2))) of approximately 60%. Oxygen uptake (V(O(2))), ventilation (V) and colonic temperature (Tc) were measured in experiments carried out at an ambient temperature of either 25 or 15 degrees C. It was found that CO hypoxia induced marked reductions in the hemoglobin O(2) half saturation pressure (P(50)). Furthermore, isolated reductions in Sa(O(2)) (with Pa(O(2)) constant) induced decreases in V(O(2)) and Tc and increases in ventilation which, as compared with normoxia, were enhanced in ambient hypoxia and reduced but still significant in hyperoxia. As suggested by previous studies, the interactions between Sa(O(2)) and Pa(O(2)) which operate on the control of metabolism and ventilation originate probably in the central nervous system.
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PMID:Metabolic and ventilatory responses to CO hypoxia at different levels of oxygenation in the rat. 1178 34

Intraoperative surgical blood loss is initially replaced by infusion of red cell-free, cristalloidal or colloidal solutions. When normovolemia is maintained the ensuing dilutional anemia is compensated by an increase of cardiac output and of arterial oxygen extraction. In the ideal case, a surgical blood loss can entirely be 'bridged' without transfusion by intraoperative normovolemic hemodilution. However major blood loss results in extreme hemodilution and the transfusion of red blood cells may finally become necessary to increase arterial oxygen content and to preserve tissue oxygenation. When transfusion has to be started before surgical control of bleeding has been achieved, parts of the red blood cells transfused will get lost, thereby increasing intraoperative transfusion needs. Beside red blood cell transfusion, arterial oxygen content can be rapidly increased by ventilating the patient with 100% oxygen (hyperoxic ventilation), thus enhancing the amount of physically dissolved oxygen in plasma (hyperoxia). In experimental and clinical studies hyperoxic ventilation has emerged as a simple, safe and effective intervention to enlarge the margin of safety for hemodynamic compensation and tissue oxygenation in hemodiluted subjects experiencing major bleeding. The hyperoxia-associated microcirculatory dysregulation and impaired tissue oxygenation known to take place in the presence of a physiologic hemoglobin concentration are not encountered in hemodiluted subjects. Hyperoxic hemodilution i.e. the combination of intraoperative extreme hemodilution and hyperoxic ventilation may therefore be considered a cost-effective, safe and efficient supplement to reduce allogeneic transfusion during surgical interventions associated with high blood losses. The vast majority of the experimental and clinical investigations this new concept is based on was initiated and performed under the guidance of Prof. Konrad Messmer.
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PMID:Hyperoxia in extreme hemodilution. 1186 21

A reduction in hemoglobin concentration has been consistently reported after deep saturation dives, whereas reductions in thrombocyte counts and changes in biochemical parameters specific for liver function have been reported after some dives. In this study the contribution of exposure to hyperoxia to these changes were studied. Hemoglobin concentration, blood cell counts, serum ferritin, and biochemical parameters specific for liver damage were measured before and after a shallow 28-day saturation dive to a pressure of 250 kPa with the same hyperoxic exposure (40-50 kPa) as in a deep saturation dive in eight male divers. The same parameters were measured before, during, and after a standard 21-day hyperbaric oxygen (HBO2) treatment series in a selected group of 16 patients (8 male). There were significant reductions in hemoglobin concentrations of 3.8 +/- 4.7% (P = 0.023) and 10.2 +/- 5.3% (P = 0.003) after the HBO2 treatment series and dive, respectively, accompanied with reductions in red cell counts, reticulocyte counts, and hematocrit. There was an increase in ferritin concentrations of 29 +/- 21% (P = 0.002) and 107 +/- 43% (P < 0.001). In contrast to some deep dives, there were no changes in thrombocyte counts or biochemical parameters specific for liver damage. Exposure to hyperoxia contributes significantly to reduced hemoglobin and increased ferritin concentrations after saturation dives. The changes may reflect a shift of iron from synthesis of hemoglobin in the bone marrow to storage in macrophages caused by a downregulation of hemoglobin synthesis, or an increased oxidative stress. The changes are too small to be of clinical significance with respect to diving and HBO2 treatment.
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PMID:Exposure to hyperoxia in diving and hyperbaric medicine--effects on blood cell counts and serum ferritin. 1190 96

Interactions of nitric oxide (NO) with hemoglobin (Hb) could regulate the uptake and delivery of oxygen (O(2)) by subserving the classical physiological responses of hypoxic vasodilation and hyperoxic vasconstriction in the human respiratory cycle. Here we show that in in vitro and ex vivo systems as well as healthy adults alternately exposed to hypoxia or hyperoxia (to dilate or constrict pulmonary and systemic arteries in vivo), binding of NO to hemes (FeNO) and thiols (SNO) of Hb varies as a function of HbO(2) saturation (FeO(2)). Moreover, we show that red blood cell (RBC)/SNO-mediated vasodilator activity is inversely proportional to FeO(2) over a wide range, whereas RBC-induced vasoconstriction correlates directly with FeO(2). Thus, native RBCs respond to changes in oxygen tension (pO2) with graded vasodilator and vasoconstrictor activity, which emulates the human physiological response subserving O(2) uptake and delivery. The ability to monitor and manipulate blood levels of NO, in conjunction with O(2) and carbon dioxide, may therefore prove useful in the diagnosis and treatment of many human conditions and in the development of new therapies. Our results also help elucidate the link between RBC dyscrasias and cardiovascular morbidity.
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PMID:Nitric oxide in the human respiratory cycle. 1272 38

The aim of the present study was to investigate whether the breathing of hyperoxic gas affects hemoglobin oxygen saturation (S(a)O(2)) and blood acidosis during intense intermittent exercise and recovery in sprint runners. The hypothesis was that the breathing of hyperoxic gas prevents S(a)O(2) from decreasing, delays blood acidosis during the exercise and improves the rate of heart rate recovery after the exercise. Nine sprinters ran three sets of 300 m at different velocities on a treadmill in normoxia (NOX) and in two hyperoxic conditions (ERHOX and RHOX; F(I)O(2) 0.40) in a randomized order. In ERHOX the inspired air was hyperoxic during the entire exercise and recovery and in RHOX the hyperoxic air was only inhaled during recovery periods. Blood pH and S(a)O(2) were measured from fingertip blood samples taken after each set of runs. The mean heart rate for the final 15 s of the last run in each set (HR(work)), the mean heart rate for the final 15 s of the first minute of recovery (HR(rec)) and the difference of HR(work) and HR(rec) (HR(dec)) were determined. In NOX, S(a)O(2) decreased from 95.0 +/- 2.0% to 88.7 +/- 2.0% (p < 0.001) but S(a)O(2) did not change in ERHOX (from 95.4 +/- 1.3% to 95.9 +/- 1.8%). A significant correlation was observed between the S(a)O(2) decrease in NOX and the effect of hyperoxia on blood pH in ERHOX (r = 0.63) and on HRdec in both ERHOX (r = 0.74) and RHOX (r = 0.69). We concluded that hemoglobin oxygen de-saturation occurred during intensive intermittent exercise in normoxia but hyperoxic gas during the exercise prevents S(a)O(2) from decreasing. Furthermore, the present results suggested that the beneficial effects of hyperoxia on heart rate recovery and blood acidosis during intensive intermittent exercise were related to hemoglobin de-saturation in normoxia.
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PMID:Effect of hyperoxia on metabolic responses and recovery in intermittent exercise. 1238 77

A giant hemangioma of the tongue was resected in a 16-year-old otherwise healthy young man (ASA I). Despite a total blood loss of 4,300 ml, corresponding to 105% of the patients intravascular blood volume, no allogeneic red blood cells had to be transfused intraoperatively. Besides minimization of intraoperative blood loss with preoperative alcohol injections into the tumor, ligation of large tumor-perfusing arteries, application of fibrin glue, skillful surgical technique, positioning of the surgical field above the level of the heart, controlled hypotension and maintenance of normothermia, acute normovolemic hemodilution (augmented by preoperative administration of recombinant human erythropoetin - rhEpo) and autotransfusion of lost blood were used for recovery of autologous blood. Under the protection of hyperoxia, a decrease of the hemoglobin (Hb) concentration to 4.2 g/dl was bridged by extreme normovolemic hemodilution. No signs of immanent or manifest tissue hypoxia were encountered. Retransfusion of autologous red blood cells was only started when surgical control of bleeding was achieved. Additionally a total of 4 units of fresh frozen plasma were infused for stabilization of plasma coagulation. After a 9-hour surgical duration, the patient was transferred to the intensive care unit, normotensive (with low-dose infusion of norepinephrin) and normothermic with a Hb concentration of 5.6 g/dl. In the face of an increasing lactacidosis 2 units of packed red blood cells were transfused on post surgical day 1.
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PMID:[Giant hemangioma of the tongue: combined use of perioperative blood conservation procedures]. 1239 34

Blood flow to contracting skeletal muscle is tightly coupled to the oxygenation state of hemoglobin. To investigate if ATP could be a signal by which the erythrocyte contributes to the regulation of skeletal muscle blood flow and oxygen (O2) delivery, we measured circulating ATP in 8 young subjects during incremental one-legged knee-extensor exercise under conditions of normoxia, hypoxia, hyperoxia, and CO+normoxia, which produced reciprocal alterations in arterial O2 content and thigh blood flow (TBF), but equal thigh O2 delivery and thigh O2 uptake. With increasing exercise intensity, TBF, thigh vascular conductance (TVC), and femoral venous plasma [ATP] augmented significantly (P<0.05) in all conditions. However, with hypoxia, TBF, TVC, and femoral venous plasma [ATP] were (P<0.05) or tended (P=0.14) to be elevated compared with normoxia, whereas with hyperoxia they tended to be reduced. In CO+normoxia, where femoral venous O2Hb and (O2+CO)Hb were augmented compared with hypoxia despite equal arterial deoxygenation, TBF and TVC were elevated, whereas venous [ATP] was markedly reduced. At peak exercise, venous [ATP] in exercising and nonexercising limbs was tightly correlated to alterations in venous (O2+CO)Hb (r2=0.93 to 0.96; P<0.01). Intrafemoral artery infusion of ATP at rest in normoxia (n=5) evoked similar increases in TBF and TVC than those observed during exercise. Our results in humans support the hypothesis that the erythrocyte functions as an O2 sensor, contributing to the regulation of skeletal muscle blood flow and O2 delivery, by releasing ATP depending on the number of unoccupied O2 binding sites in the hemoglobin molecule.
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PMID:Erythrocyte and the regulation of human skeletal muscle blood flow and oxygen delivery: role of circulating ATP. 1245 91

The effects of hyperoxia on submaximal exercise with the self-contained breathing apparatus (SCBA) were studied in 25 males. Each participant completed a graded exercise test for the determination of ventilatory threshold (VT) and then a submaximal practice trial with a normoxic gas mixture. The normoxic (20.93 +/- 0.22% O(2); SUB(21)) and hyperoxic (40.18 +/- 0.73% O(2); SUB(40)) submaximal trials were then administered in a random order. All exercise tests were completed on separate days while wearing firefighting gear and the SCBA. Compared with SUB(21), hyperoxia significantly reduced minute ventilation (V(E)), mask pressure (P(mask)), heart rate, blood lactate concentration, perceived exertion, and perceived breathing distress. As expected, hemoglobin saturation remained higher (p < 0.05) during SUB(40). The reductions in both V(E) and P(mask) with hyperoxia imply a reduction in the work of breathing during exercise. Total gas consumption was 10.3 +/- 8.1% lower during SUB(40) when compared to SUB(21), another finding that has significant practical implications for occupational safety.
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PMID:The effect of hyperoxia on submaximal exercise with the self-contained breathing apparatus. 1248 86

We hypothesized that elevated partial pressures of O(2) would increase perivascular nitric oxide (*NO) synthesis. Rodents with O(2)- and.NO-specific microelectrodes implanted adjacent to the abdominal aorta were exposed to O(2) at partial pressures from 0.2 to 2.8 atmospheres absolute (ATA). Exposures to 2.0 and 2.8 ATA O(2) stimulated neuronal (type I) NO synthase (nNOS) and significantly increased steady-state.NO concentration, but the mechanism for enzyme activation differed at each partial pressure. At both pressures, elevations in.NO concentration were inhibited by the nNOS inhibitor 7-nitroindazole and the calcium channel blocker nimodipine. Enzyme activation at 2.0 ATA O(2) appeared to be due to an altered cellular redox state. Exposure to 2.8 ATA O(2), but not 2.0 ATA O(2), increased nNOS activity by enhancing nNOS association with calmodulin, and an inhibitory effect of geldanamycin indicated that the association was facilitated by heat shock protein 90. Infusion of superoxide dismutase inhibited.NO elevation at 2.8 but not 2.0 ATA O(2). Hyperoxia increased the concentration of.NO associated with hemoglobin. These findings highlight the complexity of oxidative stress responses and may help explain some of the dose responses associated with therapeutic applications of hyperbaric oxygen.
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PMID:Stimulation of perivascular nitric oxide synthesis by oxygen. 1250 79


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