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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

Normal and iron-deficient rats were exposed to 90% O2 at 760 Torr for 24 or 48 h. Erythrocyte response to hyperoxia was monitored by potassium (rubidium) influx studies, by storage stress, and by ultrastructural studies. Normal rat erythrocytes exhibited morphological changes and decrease of ouabain-sensitive potassium influx compared to unexposed controls. Both components of erythrocyte potassium influx were affected by iron deficiency. Erythrocytes from unexposed iron-deficient rats showed a 50% increase in ouabain-sensitive potassium influx compared to controls. Iron-deficient rats exposed to hyperoxia for 24 or 48 h, had erythrocytes with morphological changes. Erythrocytes of iron-deficient rats exposed for 24 h showed no influx change; those exposed for 48 h showed a decrease of ouabain-sensitive influx compared to erythrocytes of controls.
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PMID:Response of the iron-deficient erythrocyte in the rat to hyperoxia. 64 73

Intravenous infusion of salbutamol 10 mug/min in seven healthy subjects significantly increased their ventilatory responses to inhaled CO2 in both hypoxia and hyperoxia. These changes in chemical control of breathing are unlikely to be significant when the drug is used in severe asthma but may benefit patients with acute exacerbations of chronic ventilatory failure. The infusion also increased heart rate, which was most pronounced when hypoxia was combined with hypercapnia. The infusion produced an average fall in plasma potassium from 3-99 to 3-10 mmol/l, which was associated with an increase in plasma glucose and serum insulin, suggesting that this arose from a shift of potassium from the extracellular to the intracellular space. Routine monitoring of plasma potassium and the electrocardiogram is indicated when an intravenous salbutamol infusion is used to treat severe asthma as the drug may predispose to cardiac dysrhythmias.
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PMID:Effect of intravenous infusion of salbutamol on ventilatory response to carbon dioxide and hypoxia and on heart rate and plasma potassium in normal men. 124 57

The drive to breathe in exercise is thought to result from a combination of neural and humoral factors, but the exact nature of the controlling signals is controversial. This review examines evidence suggesting that potassium could be a signal that drives ventilation (VE) in exercise. Potassium is lost from working muscle, which results in a marked hyperkalemia in the arterial plasma. The rise in potassium is directly proportional to the increase in carbon dioxide production during exercise and is also well correlated with VE in normal subjects and in subjects who do not produce acid (McArdle's syndrome). In the anesthetized and decerebrate cat, physiological levels of hyperkalemia stimulate VE by direct excitation of the peripheral arterial chemoreceptors, because surgical and chemical denervation of the chemoreceptors abolishes the increase in VE caused by potassium. The effect of hyperkalemia on chemoreceptor activity is further enhanced by hypoxia, but an abrupt switch to hyperoxia removes this effect. From these studies, it is suggested that potassium fulfills many of the criteria of being the special substance or "work factor" that was postulated over a century ago to stimulate VE in exercise. Although there is no direct proof that potassium causes an increase in breathing during exercise, circumstantial evidence strongly supports the idea that it should be considered as a stimulus to exercise hyperpnea.
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PMID:Potassium and ventilation in exercise. 131 99

The conversion of xanthine dehydrogenase (XDH) to xanthine oxidase (XO) and the reaction of XO-derived partially reduced oxygen species (PROS) have been suggested to be important in diverse mechanisms of tissue pathophysiology, including oxygen toxicity. Bovine aortic endothelial cells expressed variable amounts of XDH and XO activity in culture. Xanthine dehydrogenase plus xanthine oxidase specific activity increased in dividing cells, peaked after achieving confluency, and decreased in postconfluent cells. Exposure of BAEC to hyperoxia (95% O2; 5% CO2) for 0-48 h caused no change in cell protein or DNA when compared to normoxic controls. Cell XDH+XO activity decreased 98% after 48 h of 95% O2 exposure and decreased 68% after 48 h normoxia. During hyperoxia, the percentage of cell XDH+XO in the XO form increased to 100%, but was unchanged in air controls. Cell catalase activity was unaffected by hyperoxia and lactate dehydrogenase activity was minimally elevated. Hyperoxia resulted in enhanced cell detachment from monolayers, which increased 112% compared to controls. Release of DNA and preincorporated [8-14C]adenine was also used to assess hyperoxic cell injury and did not significantly change in exposed cells. Pretreatment of cells with allopurinol for 1 h inhibited XDH+XO activity 100%, which could be reversed after oxidation of cell lysates with potassium ferricyanide (K3Fe(CN)6). After 48 h of culture in air with allopurinol, cell XDH+XO activity was enhanced when assayed after reversal of inhibition with K3Fe(CN)6, and cell detachment was decreased. In contrast, allopurinol treatment of cells 1 h prior to and during 48 h of hyperoxic exposure did not reduce cell damage. After K3Fe(CN)6 oxidation, XDH+XO activity was undetectable in hyperoxic cell lysates. Thus, XO-derived PROS did not contribute to cell injury or inactivation of XDH+XO during hyperoxia. It is concluded that endogenous cell XO was not a significant source of reactive oxygen species during hyperoxia and contributes only minimally to net cell production of O2- and H2O2 during normoxia.
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PMID:The contribution of vascular endothelial xanthine dehydrogenase/oxidase to oxygen-mediated cell injury. 156 25

1. In response to an acute exercise-induced metabolic acidosis, the fall of arterial pH is constrained by the magnitude of the compensatory hyperventilation. To determine the role of the carotid bodies in this regulatory process, subjects performed prolonged (24 min) square-wave cycle ergometry from a background of unloaded cycling at inspired oxygen fractions (FI,O2) of 0.12 O2 (high carotid body gain), 0.21 O2 (normal carotid body gain) and 0.80 O2 (low carotid body gain). The work rates were selected to provide the same exercise intensity, despite the different inspirates; i.e. resulting in a constant increase in arterial blood [lactate] (delta [L-] approximately 4 mequiv l-1. 2. Ventilatory and pulmonary gas exchange variables were computed breath-by-breath and arterial blood was sampled at intervals throughout the tests and analysed subsequently for [lactate], [pyruvate], arterial partial pressures of oxygen and carbon dioxide (PO2, PCO2), pH, [bicarbonate] and [potassium]. 3. Hypoxia markedly reduced, and hyperoxia magnified, the transient decrease in arterial pH following exercise onset. However, there was a slow acid-base compensatory component, even when carotid chemosensitivity was suppressed by hyperoxia. We therefore conclude that, in humans, carotid body chemosensitivity plays a dominant role in constraining variations of arterial pH in response to the acute metabolic acidosis of heavy exercise, but that secondary-presumably central chemosensory-mechanisms subserve a slower compensatory role.
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PMID:Role of the carotid bodies in the respiratory compensation for the metabolic acidosis of exercise in humans. 182 63

Raising arterial potassium ([K+]a) from ca. 3.5 to 6.5 mM, as occurs in heavy exercise, excites the arterial chemoreceptors and ventilation (VE) in anaesthetised cats. We have previously shown that the excitation of chemoreceptors by potassium is enhanced by hypoxia and abolished by hyperoxia, and here we show, in decerebrate cats, that the potassium-induced increase in VE is also abolished by hyperoxia. 100% oxygen was given abruptly in hypoxia (PETO2 ca. 50 Torr), with inspired gas tensions adjusted to give the same PETO2 and PETCO2 values before all tests on a given animal. Intravenous infusions of 150 mM KCl, which raised [K+]a from 3.9 +/- 0.3 mM to 7.4 +/- 0.3 mM (mean +/- SE), always excited hypoxic VE (42 +/- 8%; P less than 0.01). Hyperoxia, given during KCl infusion, reduced VE to a value not significantly greater (P greater than 0.27) than the hyperoxic value obtained before infusion. These results show that: (i) VE reflects the responses of chemoreceptors to K+, (ii) that abrupt hyperoxia removes the potassium-induced ventilatory drive, and (iii) that, in our experiments, K+ appears to have excited VE only via the peripheral chemoreceptors.
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PMID:Effect of oxygen on potassium-excited ventilation in the decerebrate cat. 187 61

Resistance of mice to altitude, gas, hemic, tissue, mixed or hyperoxis hypoxia, to oxidative phosphorylation uncoupling agents and to X-ray irradiation during 2 days after exposure to severe acute hypobaric hypoxia was investigated. No significant changes were found in animal resistance to hemic and tissue hypoxia and to oxidative phosphorylation uncoupling agents. Resistance to hypoxic hypoxia was 2.5 times higher at the 2nd hour of the posthypoxic period and returned to the baseline by the 24 th hour. Resistance to sodium nitrite and potassium persulphate that cause hypoxia of mixed type, to hyperoxia and X-raying increased significantly by the 24th hour and returned to the baseline by the 48th hour of the posthypoxic period. The potential role of the antioxidative system in the induction of resistance to oxidative agents and X-ray irradiation during the posthypoxic period is discussed.
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PMID:[Resistance of mice to hypoxia of various types and to X-ray radiation in the post-hypoxic period]. 232 67

The contractile effects of 19 factors on isolated human arterial segments at term pregnancy were quantified, and 14 contractile agents were similarly applied to preterm (23 to 35 weeks) umbilical arteries. Responses to potassium chloride were used to normalize the data. At comparison with the term vessel, the preterm artery contracted more to angiotensin II and arachidonic acid and was more sensitive to oxytocin. Contractions were greater in term arteries to vasopressin, norepinephrine, prostaglandin D2, and prostaglandin E2 but similar in both group of arteries to bradykinin, histamine, acetylcholine, and prostaglandin F2 alpha. Neuropeptide Y, linoleic acid, uridine triphosphate, and thrombin were ineffective. Hyperoxia inconsistently induced weak, short-lived contractions. Contractions to cooling manifested marked desensitization and tachyphylaxis. Serotonin was the only agonist that displayed the pharmacodynamic features most likely to be important for closure: potency, efficacy, and long duration of action (greater than 2.5 hours). It was postulated that cellular elements surrounding umbilical vessels are primary sources of vasoactive agents that are important to closure of the fetoplacental circulation at birth.
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PMID:Pharmacodynamic study of maturation and closure of human umbilical arteries. 291 87

1. We have studied the effects of intravenous infusions of 0.1 mmol/min KCl (raising arterial potassium from ca. 3.2 to 6.0 mM) on the steady-state responses of carotid body chemoreceptors to end-tidal PCO2 and PO2 in the pentobarbitone-anaesthetized cat. 2. The excitatory effect of these KCl infusions was enhanced by hypoxia and reduced or abolished by hyperoxia. 3. Hypercapnia did not enhance, and usually reduced, excitation by KCl. 4. When similar control discharge frequencies were established by hypoxia or by hypercapnia, a KCl infusion excited the hypoxic discharge by about twice as much as it did the hypercapnic discharge. 5. These observations are not inconsistent with the idea that the mechanism underlying hypoxic excitation of arterial chemoreceptors is one that controls extracellular potassium concentration near the afferent nerve ending. 6. Insofar as potassium-induced excitation of chemoreceptor discharge is abruptly reduced by hyperoxia it behaves like Asmussen and Nielsen's postulated 'anaerobic work substance' and it may therefore contribute to the increased importance of the arterial chemoreflex reported in exercise.
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PMID:Effects of potassium, oxygen and carbon dioxide on the steady-state discharge of cat carotid body chemoreceptors. 313 72


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