Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Authors studied the behaviour of acid-base balance in subjects with chronic obstructive lung disease undergoing Maximal Aerobic Work following the method of Pasargiklian e Coll., 1955. For the research two different experimental pattern were adopted: 1) patients were subjected, in two different sessions, to the muscular work in room air and in hyperoxia (60%) breathing for the evaluation of acid-base balance. During hyperoxia Authors observed rising of paO2 and decrease of paCO2, pH and lactic acid concentration. 2) In the second pattern the muscular test was performed in room air only with the use of an antiphosphodiesterasic drug e.v. administration in each patient. Together with acid-base balance behaviour of plasmatic electrolytic assessment was controlled in order to evaluate adaptation to work. The data, although preliminary, show an increase of paO2 with decrease of paCO2 in both test; potassium and bicarbonates concentration increase more in the first test without theophyllin whereas this drug forbid these increments. The Authors even if the experimental program must be developed suggest that the evaluation of these data is interesting in diagnosis and prognosis in chronic lung disease for the cellular adaptation to work and offers interesting elements to carry on the rehabilitation of chronic obstructive lung disease.
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PMID:[Changes in the acid-base equilibrium and the water-electrolyte balance during maximum aerobic work in patients with chronic broncho-pulmonary disease]. 43 34

Several reactive oxygen intermediates are generated in biological processes involved in cellular respiration and during the respiratory burst of phagocytic cells. Exogenous insult of free radicals to respiratory tract may derive from polluting environmental agents, cigarette smoke, drugs, toxic compounds, and hyperoxia. Oxidizing radicals cause damage to proteins, lipids, carbohydrates, enzymes, nucleic acids, and other biological constituents. They are counterbalanced by different defensive mechanisms present in the body, whose action may be enhanced by exogenous antioxidant supply. Oxidants may have a role in patients with COPD, since the majority of these subjects are heavy smokers and show increased amount of highly activated phagocytes in their respiratory tract. This determines inactivation of the antiprotease system, increase in elastase production, and impairment of the connective tissue repair, so leading to structural changes that characterize chronic obstructive pulmonary disease.
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PMID:Oxidant/antioxidant imbalance: role in the pathogenesis of COPD. 157 27

We investigated the mechanisms responsible for oxygen-induced hypercarbia in ventilator-dependent patients with advanced chronic obstructive pulmonary disease (COPD). To quantitate the effects of oxygen (O2) on respiratory drive, we determined the CO2 recruitment threshold (PCO2 RT) in 10 mechanically ventilated patients under normoxic (PaO2 = 67 +/- 7 mm Hg) and hyperoxic (PaO2 = 370 +/- 67 mm Hg) conditions. PCO2 RT is a measure of the CO2 responsiveness of the mechanically unloaded respiratory system and, as such, is independent of mechanical impedance and respiratory muscle strength. After O2 supplementation, PCO2 RT increased from 42 +/- 6 to 45 +/- 6 mm Hg (p less than or equal to 0.05), indicating a suppression of so-called hypoxic respiratory drive. The effect of hyperoxia on the dead space to tidal volume ratio (VD/VT) and CO2 elimination (VCO2) was studied in 6 patients. Measurements were made at identical ventilator settings, thus eliminating breathing pattern- and respiratory work-related effects on these variables. VD/VT rose from 0.49 +/- 0.09 to 0.55 +/- 0.06 (p less than or equal to 0.05), but VCO2 remained constant at 0.21 L/min. We discuss why measuring O2-induced changes in minute ventilation, VCO2, PaO2, and VD/VT in spontaneously breathing patients is insufficient to distinguish between gas exchange- and respiratory drive-related mechanisms for hypercarbia. Based on the O2-induced increase in PCO2 RT, we conclude that so-called suppression of hypoxic drive plays an important role in the pathogenesis of this disorder.
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PMID:Oxygen-induced hypercarbia in obstructive pulmonary disease. 190 46

A 30 minute test of hyperoxia (10 l.min-1) was conducted in patients (n = 21) with chronic obstructive lung disease during the weaning trials from mechanical ventilation. Two groups were formed according to whether the occlusion pressure at 100 ms (PO.1), index of central stimulation, decreased or not during the test. The first group lowered PO.1 and increased PaCO2 by decreasing VE (minute-ventilation), VA (alveolar ventilation) and increasing the VD/VT ratio; the others had a lower PO.1 and did not modify it after administration of 02 despite a lowered PaO2 initially identical to that in the first group. They held PaCO2 constant by increasing VE and by maintaining VA in relationship with an improvement in diaphragm contractility and/or a better response to hypercapnia stimulus. All the patients is this group were successfully weaned eight days after the study period.
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PMID:[Hyperoxia test during attempts to withdraw artificial ventilation]. 278 51

We investigated the mechanism of hyperoxic-induced hypercapnia in 17 stable patients with moderate to severe chronic obstructive pulmonary disease (mean FEV1 = 0.95 L and FVC = 2.43 L). Ventilatory and mouth occlusion pressure (P0.1) responses to hypercapnia and hypoxia were measured with standard rebreathing techniques. In a randomized, single-blind fashion, we studied the effect of 15 min of hyperoxia or air on transcutaneous carbon dioxide (PtcCO2), CO2 production (VCO2), total minute ventilation (VE), and calculated dead space to tidal volume ratio (VD/VT). With O2, the PtcCO2 (p less than 0.01) and VD/VT (p less than 0.02) increased. The change in PtcCO2 with O2 was not significantly related to the indices of respiratory drive, nor to the baseline PtcCO2 or SaO2, but was related to the FEV1 (p less than 0.05). The O2 caused a slight decrease in mean VE and mean VCO2, but the effects in individual patients were variable. Both substantial increases or decreases in VE (delta VE) occurred, but these were accompanied by changes in VCO2 (delta VCO2) in the same direction. The effect of changes in VE on PaCO2 is shown to be almost completely cancelled by the concomitant changes in VCO2. Thus, the major portion of the change in PaCO2 was due to changes in VD/VT. We conclude that hyperoxic-induced hypercapnia is primarily due to impairment in gas exchange rather than to depression of ventilation. A reduced FEV1 appears to be a significant risk factor, whereas indices of respiratory drive are not likely to play a major role.
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PMID:Hyperoxic-induced hypercapnia in stable chronic obstructive pulmonary disease. 356 37

In 10 exercising patients with chronic obstructive lung disease (COLD) we measured ventilation (VE), end-tidal CO2 (PETCO2), mean inspiratory flow (VT/TI), the ratio of inspiratory time to total time for one cycle (TI/TTOT), and occlusion pressure at 0.1 s measured at the mouth (P O.1), when they breathed room air and 100% oxygen. Oxygen breathing increased the maximal work load achieved. Furthermore, at the same exercise load, P O.1, VT/TI, VE, heart rate, respiratory frequency (f) decreased significantly in hyperoxia as compared with normoxia. Thoraco-pulmonary impedance assessed by P 0.1/VE and P 0.1/(VT/TI) ratios showed a slight but significant decrease to the respiratory centre. Thus in exercising patients affected by COLD, hyperoxia not only decreases the chemical afferent drive but also may slightly reduce the afferent mechanical drive to the respiratory centre. The decrease in the thoraco-pulmonary impedance may be explained either by an increase in efficiency of the respiratory muscles and/or a decrease in airway resistance.
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PMID:Effect of oxygen on breathing during exercise in patients with chronic obstructive lung disease. 680 64

The drive and performance of breathing during hypercapnia, isocapnic hypoxia, and transient hyperoxia were studied in 20 normal children (mean age 12.3 years), in ten children with asthma, and in ten children with cystic fibrosis (CF) matched by sex and age. These latter two groups of patients had had obstructive respiratory symptoms since infancy and their pulmonary disease was of moderate severity as documented by their pulmonary function studies. During hypercapnia, normal children had a linear increase in minute ventilation (delta VE), in tidal volume (delta VT) and in the inspiratory drive (VT/Ti). The drive of breathing was evaluated by the occlusion pressure (P0.1) at functional residual capacity. The P0.1 response to PaCO2 was linear. Patients with asthma and CF showed a blunted ventilatory response (delta VE, delta VT, VT/Ti) to Co2 but a normal response in P0.1. In normal subjects, the test of isocarbic hypoxia demonstrated an exponential type of increase in delta VE, delta VT, and P0.1 as PAO2 decreased from 110 to 40 torr. With severe hypoxia (PAO2 less than 50 torr), children with CF (but not asthmatic patients) experienced a paradoxical decrease in delta VE while the drive (P0.1) remained above normal in both groups of patients. Finally, the transient O2 inhalation test caused a decrease in VE of 26%, 21%, an 34%, respectively, in normal subjects, in asthmatic children, and in children with CF. It is concluded that the CO2 and O2 drive of normal children resembles that described for adults and that the CO2 and O2 command of breathing is normal in children with asthma and CF. However, the ventilatory response in children with chronic obstructive pulmonary disease is subnormal probably due to the impairment of the respiratory mechanics. Finally the respiratory depression induced by severe hypoxia in children with CF is unexplained, but it may reflect the high dependency of their respiratory muscle on oxygen supply.
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PMID:Neural drive and ventilatory strategy of breathing in normal children, and in patients with cystic fibrosis and asthma. 726 24

Our aim was to evaluate the efficacy of assisted ventilation through a nasal mask (AVN) in treating chronic obstructive pulmonary disease (COPD) patients who were admitted to a pneumology ward due to decompensation, with PaCO2 > 60 mmHg and pH < 7.35. We studied 13 COPD patients who were first observed for 1-2 days until adaptation and then given 2 daily sessions of AVN lasting 4 hours with double positive pressure (DP90) devices through Sullivan mask with a cannula for hyperoxia. Gasometric readings were recorded, along with subjective assessment of condition and problems with the mask. Gasometric readings were taken as follows: the first upon admission to the ward (AW), the second with AVN 2 days after adaptation and the third 3 hours after the second (POST). Statistical analysis was with a Student t-test for paired series. Mean age was 64 +/- 3 years and FEV1 was 0.69 +/- 0.14 l. Interruptions were due to the need for mouth opening even at minimum pressures, and the inability to adapt to the consequent tachypnea. No other problems were reported by the remaining patients and all perceived improvement subjectively. The pH of 7.29 +/- 0.03 at AW increased to 7.41 +/- 0.03 with AVN (p < 0.001) and held steady at 7.39 +/- 0.01 at POST (p < 0.001 POST-AW and p = NS POST-AVN). PaO2/FiO2 was 223 +/- 49 mmHg at AW and 267 +/- 41 mmHg at the POST reading (p = 0.06). PaO2 with AVN was 67 +/- 8 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Assisted ventilation via nasal mask in patients hospitalized in a pneumology ward for decompensation of their chronic air-flow obstruction]. 758 31

Despite the absence of cardiac or renal pathologies, edema and mild hyponatremia may often occur in patients affected by chronic obstructive pulmonary disease (COPD). Therefore, it has been suggested that hypoxia may influence the release of different hormones regulating renal sodium handling. To evaluate the effect of hyperoxia and O2 removal on plasma digitalis-like substance (DLS) levels, 9 patients affected by COPD and 7 normal subjects were studied. After 1 h in supine position, O2 was administered for 3 h by a tight-fitting face-mask. Blood samples for plasma DLS were taken at time 0, 60, 180 min and then for 3 h after O2 removal. In normal subjects, plasma DLS did not vary after O2 administration (from basal values of 162.25 +/- 8.59 to 107.75 +/- 6.65 pg/ml at 180 min; NS), and O2 removal (143.7 +/- 16.87 pg/ml after 3 h from O2 removal; NS). On the contrary, in patients affected by COPD, plasma DLS levels increased during O2 administration (from basal values of 138.98 +/- 8.31 to 202.14 +/- 8.21 pg/ml at 180 min; p < 0.05), and returned to baseline levels (142.59 +/- 8.28 pg/ml) 3 h after O2 removal. In the same patients, DLS increase was accompanied by a rise in Na+ excretion (from 0.08 +/- 0.01 at time 0 to 0.16 +/- 0.02 mEq/min after 3 h of O2 administration; p < 0.05). In conclusion, our findings showed an oxygen-related increase in plasma DLS levels and in urinary Na+ excretion in patients affected by COPD. This phenomenon could promote Na+ urinary loss during prolonged O2 therapy in these patients and should be taken into account in their management.
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PMID:Oxygen administration increases plasma digoxin-like substance and renal sodium excretion in chronic hypoxic patients. 821 27

Patients with severe chronic obstructive pulmonary disease (COPD) are limited in their exercise tolerance by the level of ventilation (VE) they can sustain. We determined whether acutely increasing blood bicarbonate levels decreased acid stimulation to the respiratory chemoreceptors during exercise, thereby improving exercise tolerance. Responses were compared with those obtained during 100% O2 breathing (known to reduce VE in these patients) and to the responses of healthy young subjects. Participants were six patients with severe COPD (forced expired volume in 1 s = 31 +/- 11% predicted) but without chronic CO2 retention and 5 healthy young subjects. Each subject performed three incremental cycle ergometer exercise tests: 1) control, 2) after ingestion of 0.3 g.kg-1 of sodium bicarbonate and 3) while breathing 100% O2. During these tests VE was measured continuously and arterialized venous blood (patients) or arterial blood (healthy subjects) was sampled serially to assess acid base variables. Bicarbonate loading increased standard bicarbonate by 4-6 mmol.L-1 and this elevation persisted during exercise. In both groups, bicarbonate loading resulted in a substantially higher arterial pH; arterial PCO2 was either unchanged (healthy subjects) or mildly (averaging 5 torr) higher (COPD patients). However, in neither group did bicarbonate loading result in an altered VE response to exercise or an increase in exercise tolerance. In contrast, superimposing hyperoxia on bicarbonate ingestion yielded, on average, 24% reduction in VE and 50% increase in peak work rate in the patients (but not in the healthy young subjects). We conclude that acute bicarbonate loading is not an ergogenic aid in patients with severe COPD.
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PMID:Effect of acute bicarbonate administration on exercise responses of COPD patients. 921 99


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