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

Recent data demonstrate that the magnitude of the heat loss that occurs from the respiratory tract during exercise correlates with the degree of post-exertional obstruction that develops in asthmatics. Respiratory heat loss relates directly to the minute ventilation and heat capacity of the inspired gas and inversely to its water content and temperature. Because it has been shown that inhaling 100% oxygen during exercise blunts the obstructive response, we wondered if this effect could be accounted for by differing values of heat exchange with air and oxygen breathing. To examine this question, we studied 10 asthmatics by measuring multiple aspects of pulmonary mechanics before and after four bouts of exhausting leg work during which the subjects inhaled either air or oxygen conditioned to provide widely differing thermal burdens on their airways. Under all inspired gas conditions, oxygen breathing produced significantly less obstruction than air. Minute ventilation was also significantly less with oxygen as was the total heat lost. As the latter fell, so did the magnitude of the postexercise obstruction. When the differences in ventilation and respiratory heat loss between air and oxygen were eliminated by eucapnic hyperventilation, the differences in the obstructive responses also disappeared. Thus, the effects of hyperoxia on exercise-induced asthma can be accounteed for solely by alterations in heat exchange.
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PMID:A critical assessment of the mechanism by which hyperoxia attenuates exercise-induced asthma. 45 67

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 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

In humans, attenuating carotid chemoreceptor activity by hyperoxia does not alter arterial PCO2 (PaCO2) during submaximal exercise, yet a transient hypercapnia occurs in carotid chemoreceptor-resected (CBR) asthmatic subjects during submaximal exercise. We hypothesized that this difference was due to asthma and not CBR causing the abnormal response. Accordingly, we determined the temporal pattern of PaCO2 during mild and moderate exercise in chemoreceptor-intact asthmatic (n = 10) and nonasthmatic subjects (n = 10). We also hypothesized that hyperoxia alters PaCO2 during exercise if exercise already has disrupted PaCO2 homeostasis. Accordingly, we studied, during exercise, asthmatic subjects while hyperoxic; nonasthmatic subjects during loaded breathing of room air, which increased PaCO2; and nonasthmatic subjects during loaded breathing while hyperoxic. While breathing room air, neither asthmatic nor nonasthmatic subjects maintained arterial isocapnia during exercise. An increase in PaCO2 between rest and exercise and between mild exercise and 1st min of moderate exercise was greater in asthmatic than in nonasthmatic subjects (P < 0.05). In six asthmatic subjects that were hypercapnic breathing room air during exercise, hypercapnia was accentuated by hyperoxia. The ventilatory load in nonasthmatic subjects resulted in a work load-dependent hypercapnia (P < 0.01) accentuated (P < 0.01) by hyperoxia. We conclude that normally in humans the carotid chemoreceptors contribute minimally to the hyperpnea of submaximal exercise. However, when PaCO2 is increased from resting values during exercise, then the chemoreceptors serve to augment ventilation and thereby minimize the hypercapnia.
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PMID:Effect of asthma and ventilatory loading on arterial PCO2 of humans during submaximal exercise. 771 39

Airway hyperreactivity is recognized as one of the long-term sequelae of bronchopulmonary dysplasia (BPD). Due to the improved care and prognosis of very low-birth weight infants, the incidence of BPD is increasing. There are data that suggest the increased survival of premature infants may be associated with the observed increased incidence of childhood asthma. The hyperoxia received as part of the treatment of respiratory distress syndrome is believed to be partly if not completely responsible for BPD. To gain insight into the potential role that hyperoxia might play in producing airway hyperreactivity, 4-day-old guinea pig pups were exposed to 70% oxygen or air for 96 h, and airway responsiveness to acetylcholine (ACh) was assessed both 2 and 9 days after the completion of the hyperoxia exposures. Unlike ozone, the mechanism for the persistently increased airway reactivity is not related either to the inhibition of neuronal acetylcholinesterase or inhibition of the neuronal M2 muscarinic receptor. A difference in antioxidant protection did not account for the increased response of the neonatal guinea pigs compared with hyperoxia-exposed rat pups. These data support the usefulness of the neonatal guinea pig as a model to study the mechanism responsible for hyperoxia-induced airway hyperreactivity.
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PMID:Airway hyperreactivity produced by short-term exposure to hyperoxia in neonatal guinea pigs. 922 25

Extensive research efforts during the last three decades resulted in a large body of experimental evidence that suggests an important role of the disbalance between generation and elimination of the oxygen and xenobiotic derived free radicals in physiological and pathological processes. Reactive oxygen species (ROS) are generated in many metabolic pathways, and are entering the organisms from exogenous sources, dominantly via airways and gut. ROS induced injuries, e.g. thermal, chemical, radiation, ischaemia/reperfusion, inflammation, hyperoxia, etc., result in diseases like atherosclerosis, ulcerative colitis, autoimmune diseases, asthma, etc. The current paper is designed to provide an overview of the effects ROS may exert in various tissues. Because of the effective defense systems, the tolerance of viable human cells to ROS is relatively high. The oxidant stress induced dysfunction of various systems, such as the gut, airways, nervous, cardiovascular system, etc., involve both direct and indirect mechanisms. Understanding of these molecular mechanisms is essential for a rational antioxidant therapy.
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PMID:Reactive oxygen species as mediators of tissue protection and injury. 1070 13

These studies examine the effect of acute hypoxia on airway smooth muscle relaxation in response to salbutamol in vitro in human isolated bronchi from non-asthmatics and in vivo in-patients with asthma. Isometric responses were measured from rings of human bronchi pre-constricted with methacholine under oxygen tensions of 95% (hyperoxia), 20% (normoxia) and 4% (hypoxia). Once contractions had plateaued, concentration - response curves were conducted to salbutamol (10(-9)-10(-4)m). Twelve stable asthmatic patients were studied in a randomised double blind fashion. On two study days following baseline measurements, patients were randomised to receive either oxygen (FiO(2)1.0) or a hypoxic gas mixture (FiO(2)0.15) followed by three incremental doses of nebulised salbutamol at 15 min intervals. On two further study days nebulised saline was administered instead of salbutamol. In isolated bronchi, salbutamol-induced relaxations were significantly (P< 0.001) greater in hyperoxia and normoxia (P< 0.01) when compared to hypoxia. Among patients with asthma no significant differences were found in the mean maximum % change in forced expiratory volume (FEV(1)) from baseline between the hypoxic and hyperoxic study days on which nebulised salbutamol was administered. We conclude that acute hypoxia attenuates airway smooth muscle relaxation in response to salbutamol in vitro but has no effect on salbutamol-induced bronchodilation in in-patients with asthma.
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PMID:The effect of acute alteration in oxygen tension on the bronchodilator response to salbutamol in vitro and in vivo in man. 1127 90

Chronic inflammation predisposes toward many types of cancer. Chronic bronchitis and asthma, for example, heighten the risk of lung cancer. Exactly which inflammatory mediators (e.g., oxidant species and growth factors) and lung wound repair processes (e.g., proangiogenic factors) enhance pulmonary neoplastic development is not clear. One approach to uncover the most relevant biochemical and physiological pathways is to identify genes underlying susceptibilities to inflammation and to cancer development at the same anatomic site. Mice develop lung adenocarcinomas similar in histology, molecular characteristics, and histogenesis to this most common human lung cancer subtype. Over two dozen loci, called Pas or pulmonary adenoma susceptibility, Par or pulmonary adenoma resistance, and Sluc or susceptibility to lung cancer genes, regulate differential lung tumor susceptibility among inbred mouse strains as assigned by QTL (quantitative trait locus) mapping. Chromosomal sites that determine responsiveness to proinflammatory pneumotoxicants such as ozone (O3), particulates, and hyperoxia have also been mapped in mice. For example, susceptibility QTLs have been identified on chromosomes 17 and 11 for O3-induced inflammation (Inf1, Inf2), O3-induced acute lung injury (Aliq3, Aliq1), and sulfate-associated particulates. Sites within the human and mouse genomes for asthma and COPD phenotypes have also been delineated. It is of great interest that several susceptibility loci for mouse lung neoplasia also contain susceptibility genes for toxicant-induced lung injury and inflammation and are homologous to several human asthma loci. These QTLs are described herein, candidate genes are suggested within these sites, and experimental evidence that inflammation enhances lung tumor development is provided.
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PMID:Susceptibility to neoplastic and non-neoplastic pulmonary diseases in mice: genetic similarities. 1535 60

Airway hyperreactivity is one of the hallmarks of hyperoxic lung injury in early life. As neurotrophins such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) are potent mediators of neuronal plasticity, we hypothesized that neurotrophin levels in the pulmonary system may be disturbed by hyperoxic exposure. We therefore evaluated the effects of hyperoxia on the expression of BDNF, NGF, and their corresponding high-affinity receptors, TrkB and TrkA, respectively, in the lung of rat pups. Five-day-old Sprague-Dawley rat pups were randomized to hyperoxic or control groups and then continuously exposed to hyperoxia (>95% oxygen) or normoxia over 7 days. At both mRNA and protein levels, BDNF was detected in lung but not in trachea; its level was substantially enhanced in lungs from the hyperoxia-exposed rat pups. Distribution of BDNF mRNA by in situ hybridization indicates that peribronchial smooth muscle was the major source of increased BDNF production in response to hyperoxic exposure. Interestingly, hyperoxia-induced elevation of BDNF was not accompanied by any changes of NGF levels in lung. Furthermore, hyperoxic exposure increased the expression of TrkB in peribronchial smooth muscle but had no effect on the distribution of the specific NGF receptor TrkA. These findings indicate that hyperoxic stress not only upregulates BDNF at mRNA and protein levels but also enhances TrkB within peribronchial smooth muscle. However, there was no corresponding effect on NGF and TrkA receptors. We speculate that the increased level of BDNF may contribute to hyperoxia-induced airway hyperresponsiveness in early postnatal life.
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PMID:Hyperoxia enhances brain-derived neurotrophic factor and tyrosine kinase B receptor expression in peribronchial smooth muscle of neonatal rats. 1582 Oct 16

Prolonged hyperoxia, as may be used to treat patients with severe hypoxemia, can lead to lung injury, respiratory failure, and death. Resident mast cells play important roles in regulating the lung response to changing environmental conditions, as evidenced by their roles in asthma and airway hyperresponsiveness. In this study we evaluated the effect of prolonged hyperoxia on the number and distribution of mast cells in the rat lung. In rats maintained in normoxia, mast cells were distributed primarily in the loose connective tissue surrounding large bronchioles and vessels of the lung. In rats exposed to normobaric hyperoxia for 72 hr, mast cell number in lung sections increased significantly, and mast cells were found preferentially accumulated around vessels throughout the lung. Notably, mast cells around smaller vessels were abundant in hyperoxic lungs but rare in normoxic lungs. Also, mast cells were increased in the pleura of lungs exposed to hyperoxia. These changes in mast cell number and distribution in response to hyperoxia were evident in aged (22-month-old) rats as well as young (3-month-old) rats. As mast cell-derived mediators have many effects, e.g., on vascular leak and vascular tone, positioning of increased mast cell numbers throughout the lung vasculature may be an important contributor to changes in lung function subsequent to persistent hyperoxia.
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PMID:Prolonged exposure to hyperoxia increases perivascular mast cells in rat lungs. 1689 61


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