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Journal articles on the topic 'Hyperoxie'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 March 2025

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1

Demiselle, Julien, Peter Radermacher, and Pierre Asfar. "Hyperoxie en réanimation." Anesthésie & Réanimation 5, no. 2 (2019): 91–97. http://dx.doi.org/10.1016/j.anrea.2018.12.003.

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2

Payen, Didier. "Hyperoxie : un réel enjeu ?" Anesthésie & Réanimation 4, no. 2 (2018): 134–37. http://dx.doi.org/10.1016/j.anrea.2017.12.011.

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3

Grafen, Keren. "Wenn die Luft in den Zellen dünn wird." Deutsche Heilpraktiker-Zeitschrift 16, no. 06 (2021): 48–52. http://dx.doi.org/10.1055/a-1523-9205.

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SummaryBei einem Sauerstoffmangel setzt der Organismus einen Mechanismus in Gang, der unter anderem durch Anpassung der Energiegewinnung für ein möglichst langes Überleben sorgen soll. Die Intervall-Hypoxie-Hyperoxie-Therapie (IHHT) setzt Hypoxie in Intervallen gezielt ein, um insbesondere Prozesse der verbesserten Energiegewinnung anzuregen, wodurch wiederum Beschwerden reduziert werden sollen. Die Intervall-Hypoxie-Hyperoxie-Therapie (IHHT) kann zum einen bei Beschwerden wie Fatigue helfen, zum anderen aber auch als Höhentraining vor Aufenthalten in hohen Bergen dienen.

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Francony, G., P. Bouzat, J. Picard, M. C. Fevre, S. Gay, and J. F. Payen. "Hyperoxie normobarique chez le patient traumatisé crânien." Annales Françaises d'Anesthésie et de Réanimation 31, no. 3 (2012): 224–27. http://dx.doi.org/10.1016/j.annfar.2011.11.009.

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5

Berger, Marc, Franziska Macholz, Peter Schmidt, and Ragnar Huhn. "Hyperoxie in Anästhesie und Intensivmedizin – Zu viel des Guten?" AINS - Anästhesiologie · Intensivmedizin · Notfallmedizin · Schmerztherapie 51, no. 06 (2016): 372–77. http://dx.doi.org/10.1055/s-0041-105156.

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6

Schmidt, S., W. Decleer, S. Gorissen-Bosselmann, et al. "Laserspektroskopische Erfassung der induzierten Hyperoxie – eine tierexperimentelle Studie beim Lamm - Laser-spectroscopy of Induced Hyperoxia – An Experimental Study in the Lamb." Biomedizinische Technik/Biomedical Engineering 35, no. 9 (1990): 185–89. http://dx.doi.org/10.1515/bmte.1990.35.9.185.

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7

Sadek, A., R. Khattab, A. Amer, and A. Youssef. "Protective role of caffeine versus N-acetylcysteine in hyperoxic acute lung injury in neonatal rats." Journal of Morphological Sciences 34, no. 02 (2017): 058–67. http://dx.doi.org/10.4322/jms.113617.

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Abstract Introduction: Prolonged breathing of high oxygen concentration leads to hyperoxic acute lung injury. Neonatal Respiratory diseases usually require increased supplement of high oxygen concentrations, so neonates are more susceptible to hyperoxic acute lung injury. The aim of this work was to investigate the protective role of caffeine versus N-acetylcysteine against hyperoxic acute lung injury in neonatal rats. Materials and Methods: 32 albino rats aged seven days were used in this experiment. The pups were divided into four groups; 1) Control or normoxic group; rats placed in normoxic

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Xu, Dong, Jill R. Guthrie, Sherry Mabry, Thomas M. Sack, and William E. Truog. "Mitochondrial aldehyde dehydrogenase attenuates hyperoxia-induced cell death through activation of ERK/MAPK and PI3K-Akt pathways in lung epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 5 (2006): L966—L975. http://dx.doi.org/10.1152/ajplung.00045.2006.

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Oxygen toxicity is one of the major risk factors in the development of the chronic lung disease or bronchopulmonary dysplasia in premature infants. Using proteomic analysis, we discovered that mitochondrial aldehyde dehydrogenase (mtALDH or ALDH2) was downregulated in neonatal rat lung after hyperoxic exposure. To study the role of mtALDH in hyperoxic lung injury, we overexpressed mtALDH in human lung epithelial cells (A549) and found that mtALDH significantly reduced hyperoxia-induced cell death. Compared with control cells (Neo-A549), the necrotic cell death in mtALDH-overexpressing cells (m

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9

Pournaras, C., K. Strommer, C. Riva, M. Tsacopoulos, and N. Gilodi. "Gradients d'O2dans la rétine du porc-miniature en normoxie et hyperoxie." Klinische Monatsblätter für Augenheilkunde 190, no. 04 (1987): 383–84. http://dx.doi.org/10.1055/s-2008-1050418.

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10

Yao, Qin, Musa A. Haxhiu, Syed I. Zaidi, Shijian Liu, Anjum Jafri, and Richard J. Martin. "Hyperoxia enhances brain-derived neurotrophic factor and tyrosine kinase B receptor expression in peribronchial smooth muscle of neonatal rats." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 2 (2005): L307—L314. http://dx.doi.org/10.1152/ajplung.00030.2005.

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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

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11

Buckley, S., W. Shi, L. Barsky та D. Warburton. "TGF-β signaling promotes survival and repair in rat alveolar epithelial type 2 cells during recovery after hyperoxic injury". American Journal of Physiology-Lung Cellular and Molecular Physiology 294, № 4 (2008): L739—L748. http://dx.doi.org/10.1152/ajplung.00294.2007.

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Hyperoxic rats treated with inosine during oxygen exposure have increased levels of active transforming growth factor (TGF)-β in the bronchoalveolar lavage (BAL), yet alveolar epithelial type 2 cells (AEC2) isolated from these animals demonstrate less hyperoxia-induced DNA damage and increased expression of active Smad2. To determine whether TGF-β1 signaling per se protected AEC2 against hyperoxic damage, freshly isolated AEC2 from hyperoxic rats were incubated with TGF-β1 for 24 h and assayed for DNA damage by fluorescein-activated cell sorter analysis of TdT-mediated dUTP nick end labeling.

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Dean, Jay B., Daniel K. Mulkey, Richard A. Henderson, Stephanie J. Potter, and Robert W. Putnam. "Hyperoxia, reactive oxygen species, and hyperventilation: oxygen sensitivity of brain stem neurons." Journal of Applied Physiology 96, no. 2 (2004): 784–91. http://dx.doi.org/10.1152/japplphysiol.00892.2003.

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Hyperoxia is a popular model of oxidative stress. However, hyperoxic gas mixtures are routinely used for chemical denervation of peripheral O2 receptors in in vivo studies of respiratory control. The underlying assumption whenever using hyperoxia is that there are no direct effects of molecular O2 and reactive O2 species (ROS) on brain stem function. In addition, control superfusates used routinely for in vitro studies of neurons in brain slices are, in fact, hyperoxic. Again, the assumption is that there are no direct effects of O2 and ROS on neuronal activity. Research contradicts this assum

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Cucchiaro, Giovanni, Arthur H. Tatum, Michael C. Brown, Enrico M. Camporesi, John W. Daucher, and Tawfic S. Hakim. "Inducible nitric oxide synthase in the lung and exhaled nitric oxide after hyperoxia." American Journal of Physiology-Lung Cellular and Molecular Physiology 277, no. 3 (1999): L636—L644. http://dx.doi.org/10.1152/ajplung.1999.277.3.l636.

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The effect of hyperoxia on nitric oxide (NO) production in intact animals is unknown. We described the effects of hyperoxia on inducible nitric oxide synthase (iNOS) expression and NO production in the lungs of rats exposed to high concentrations of oxygen. Animals were placed in sealed Plexiglas chambers and were exposed to either 85% oxygen (hyperoxic group) or 21% oxygen (negative control group). Animals were anesthetized after 24 and 72 h of exposure and were ventilated via a tracheotomy. We measured NO production in exhaled air (ENO) by chemiluminescence. The lungs were then harvested and

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Thimonier, C., V. Deral-Stephant, P. Daubas, and L. Bourdon. "469 Comparaison de l’ERG multifocal en hyperoxie, entre sujets sportifs et sédentaires." Journal Français d'Ophtalmologie 32 (April 2009): 1S146. http://dx.doi.org/10.1016/s0181-5512(09)73593-4.

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15

Prieur, F., G. Dupont, D. Renard, and P. Mucci. "Évolution de l’oxygénation musculaire au début de l’exercice intense en hyperoxie modérée." Science & Sports 22, no. 6 (2007): 302–4. http://dx.doi.org/10.1016/j.scispo.2007.09.006.

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16

Sutherland, Megan R., Megan O'Reilly, Kelly Kenna, et al. "Neonatal hyperoxia: effects on nephrogenesis and long-term glomerular structure." American Journal of Physiology-Renal Physiology 304, no. 10 (2013): F1308—F1316. http://dx.doi.org/10.1152/ajprenal.00172.2012.

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Preterm neonates are born while nephrogenesis is ongoing and are commonly exposed to factors in the extrauterine environment that may impair renal development. Supplemental oxygen therapy exposes the preterm infant to a hyperoxic environment that may induce oxidative stress. Our aim was to determine the immediate and long-term effects of exposure to hyperoxia, during the period of postnatal nephrogenesis, on renal development. Newborn mice (C57BL/6J) were kept in a normoxic (room air, 21% oxygen) or a controlled hyperoxic (65% oxygen) environment from birth to postnatal day 7 ( P7d). From P7d,

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17

Thiruvenkataramani, Ranga Prasanth, Amal Abdul-Hafez, Ira Gewolb, and Bruce Uhal. "Mas Receptor Agonist AVE0991 increases surfactant protein expression under hyperoxic conditions in human lung epithelial cells." Journal of Lung, Pulmonary & Respiratory Research 7, no. 4 (2020): 85–91. http://dx.doi.org/10.15406/jlprr.2020.07.00235.

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Background: Hyperoxia in pre-term neonates is a known risk factor of bronchopulmonary dysplasia (BPD). Hyperoxia is known to cause oxidative stress, inflammatory changes that leads to surfactant deactivation, and decreased surfactant expression. The previous research has shown short term exposure to hyperoxia increases surfactant protein expression but decreased expression in long term exposure. Local tissue renin-angiotensin system (RAS) is associated with tissue injury and repair and it may play a role in BPD. Endogenous peptide angiotensin 1-7 acts on the MAS receptor. The activation of the

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18

Kawamura, Tomohiro, Nobunao Wakabayashi, Norihisa Shigemura, et al. "Hydrogen gas reduces hyperoxic lung injury via the Nrf2 pathway in vivo." American Journal of Physiology-Lung Cellular and Molecular Physiology 304, no. 10 (2013): L646—L656. http://dx.doi.org/10.1152/ajplung.00164.2012.

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Hyperoxic lung injury is a major concern in critically ill patients who receive high concentrations of oxygen to treat lung diseases. Successful abrogation of hyperoxic lung injury would have a huge impact on respiratory and critical care medicine. Hydrogen can be administered as a therapeutic medical gas. We recently demonstrated that inhaled hydrogen reduced transplant-induced lung injury and induced heme oxygenase (HO)-1. To determine whether hydrogen could reduce hyperoxic lung injury and investigate the underlying mechanisms, we randomly assigned rats to four experimental groups and admin

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19

Schauer, Steven G., Michael D. April, Jason F. Naylor, et al. "Incidence of Hyperoxia in Combat Wounded in Iraq and Afghanistan: A Potential Opportunity for Oxygen Conservation." Military Medicine 184, no. 11-12 (2019): 661–67. http://dx.doi.org/10.1093/milmed/usz125.

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Abstract Introduction Oxygen supplementation is frequently used in critically injured trauma casualties in the combat setting. Oxygen supplies in the deployed setting are limited so excessive use of oxygen may unnecessarily consume this limited resource. We describe the incidence of supraphysiologic oxygenation (hyperoxia) within casualties in the Department of Defense Trauma Registry (DoDTR). Methods This is a subanalysis of previously published data from the DoDTR – we isolated casualties with a documented arterial blood gas (ABG) and categorized hyperoxia as an arterial oxygen &gt;100 m

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Chen, Yin, Dong Wei, Jin Zhao, Xiangnan Xu, and Jingyu Chen. "Reduction of hyperoxic acute lung injury in mice by Formononetin." PLOS ONE 16, no. 1 (2021): e0245050. http://dx.doi.org/10.1371/journal.pone.0245050.

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Background The antioxidant and anti-inflammatory features of Formononetin, an isoflavone constituent extracted from traditional Chinese medicine, have been reported. The present study investigated that whether Formononetin plays a benefit on hyperoxic ALI. Methods C57BL/6 mice were exposed to hyperoxia for 72 h to produce experimental hyperoxic ALI model. Formononetin or vehicle was administrated intraperitoneally. Samples from the lung were collected at 72 h post hyperoxia exposure for further study. Pulmonary microvascular endothelial cells isolated from the lung of C57BL/6 mice were used fo

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Agani, F. H., N. T. Kuo, C. H. Chang, et al. "Effect of hyperoxia on substance P expression and airway reactivity in the developing lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 273, no. 1 (1997): L40—L45. http://dx.doi.org/10.1152/ajplung.1997.273.1.l40.

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This study was undertaken to characterize changes in the tachykinin system induced by hyperoxic exposure and the potential effects on airway contractile responses. We exposed 7-day-old rat pups to either room air or hyperoxia (> 95% O2) for 7 days to assess pulmonary beta-preprotachykinin (beta-PPT) gene expression, substance P (SP) levels, and airway contractile responses to cholinergic stimulation before and after neurokinin-1 (NK1) receptor blockade. Lung beta-PPT mRNA expression, lung and tracheal SP levels, and contractile responses to exogenous acetylcholine and electrical field stimu

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Sopi, Ramadan B., Richard J. Martin, Musa A. Haxhiu, et al. "Role of brain-derived neurotrophic factor in hyperoxia-induced enhancement of contractility and impairment of relaxation in lung parenchyma." American Journal of Physiology-Lung Cellular and Molecular Physiology 295, no. 2 (2008): L348—L355. http://dx.doi.org/10.1152/ajplung.00067.2008.

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Prolonged hyperoxic exposure contributes to neonatal lung injury, and airway hyperreactivity is characterized by enhanced contraction and impaired relaxation of airway smooth muscle. Our previous data demonstrate that hyperoxia in rat pups upregulates expression of brain-derived neurotrophic factor (BDNF) mRNA and protein, disrupts NO-cGMP signaling, and impairs cAMP production in airway smooth muscle. We hypothesized that BDNF-tyrosine kinase B (TrkB) signaling plays a functional role in airway hyperreactivity via upregulation of cholinergic mechanisms in hyperoxia-exposed lungs. Five-day-old

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Bartman, Colleen M., Daniel Wasim Awari, Christina M. Pabelick, and Y. S. Prakash. "Intermittent Hypoxia-Hyperoxia and Oxidative Stress in Developing Human Airway Smooth Muscle." Antioxidants 10, no. 9 (2021): 1400. http://dx.doi.org/10.3390/antiox10091400.

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Premature infants are frequently and intermittently administered supplemental oxygen during hypoxic episodes, resulting in cycles of intermittent hypoxia and hyperoxia. The relatively hypoxic in utero environment is important for lung development while hyperoxia during the neonatal period is recognized as detrimental towards the development of diseases such as bronchopulmonary dysplasia and bronchial asthma. Understanding early mechanisms that link hypoxic, hyperoxic, and intermittent hypoxic-hyperoxic exposures to altered airway structure and function are key to developing advanced therapeuti

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Reydellet, Laurent, Audrey Le Saux, Valery Blasco, et al. "Impact of Hyperoxia after Graft Reperfusion on Lactate Level and Outcomes in Adults Undergoing Orthotopic Liver Transplantation." Journal of Clinical Medicine 12, no. 8 (2023): 2940. http://dx.doi.org/10.3390/jcm12082940.

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Background: Hyperoxia is common during liver transplantation (LT), without being supported by any guidelines. Recent studies have shown the potential deleterious effect of hyperoxia in similar models of ischemia–reperfusion. Hyperoxia after graft reperfusion during orthotopic LT could increase lactate levels and worsen patient outcomes. Methods: We conducted a retrospective and monocentric pilot study. All adult patients who underwent LT from 26 July 2013 to 26 December 2017 were considered for inclusion. Patients were classified into two groups according to oxygen levels before graft reperfus

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Singhal, Aneesh B., Xiaoying Wang, and Eng H. Lo. "Effects of Normobaric Hyperoxia in a Rat Model of Transient Focal Cerebral Ischemia and Reperfusion." Stroke 32, suppl_1 (2001): 316. http://dx.doi.org/10.1161/str.32.suppl_1.316-b.

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3 Background: The role of therapeutic oxygen in treatment of acute stroke is controversial. Oxygen improves cellular aerobic metabolism and can salvage ischemic tissue. However, oxygen free radicals can increase blood brain barrier (BBB) damage, and oxygen can induce vasoconstriction, which could worsen stroke outcome. We studied the effects of normobaric oxygen in cerebral ischemia and reperfusion. Methods: Rats were subjected to normobaric hyperoxia (FiO2 100%) or normoxia (FiO2 30%) during two hour filament occlusion and one hour reperfusion of the middle cerebral artery. Twenty-four hour i

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Patel, Vivek, Katelyn Dial, Jiaqi Wu, et al. "Dietary Antioxidants Significantly Attenuate Hyperoxia-Induced Acute Inflammatory Lung Injury by Enhancing Macrophage Function via Reducing the Accumulation of Airway HMGB1." International Journal of Molecular Sciences 21, no. 3 (2020): 977. http://dx.doi.org/10.3390/ijms21030977.

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Mechanical ventilation with hyperoxia is the major supportive measure to treat patients with acute lung injury and acute respiratory distress syndrome (ARDS). However, prolonged exposure to hyperoxia can induce oxidative inflammatory lung injury. Previously, we have shown that high levels of airway high-mobility group box 1 protein (HMGB1) mediate hyperoxia-induced acute lung injury (HALI). Using both ascorbic acid (AA, also known as vitamin C) and sulforaphane (SFN), an inducer of nuclear factor (erythroid-derived 2)-like 2 (Nrf2), we tested the hypothesis that dietary antioxidants can mitiga

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Suchý, Jiří, Jiří Novotný, and Pavel Tilinger. "Porovnání vlivu hyperoxie na krátkodobý anaerobní výkon v nížině a vyšší nadmořské výšce." Studia sportiva 4, no. 1 (2010): 17–23. http://dx.doi.org/10.5817/sts2010-1-3.

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The article compares the infl uence of inhaling concentrated oxygen on short-term repeated performance in lowlands and at high altitudes above sea level (1 835 m a.s.l.). Th e source of concentrated oxygen was Oxyfi t. Th e subjects (n=10) completed a total of four tests comprised of two Wingate tests at a 10 minute interval. Two tests were carried out at a low altitude and two at a higher altitude above sea level. During the recovery period between tests the monitored subjects inhaled Oxyfi t or a placebo (at both the low and high altitudes). Th e study showed signifi cantly (p < 0.05) hig

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Pournaras, C., J. Munoz, and R. Abdesselem. "Régulation de la PO2au niveau de la papille du porc miniature en hyperoxie*." Klinische Monatsblätter für Augenheilkunde 198, no. 05 (1991): 404–5. http://dx.doi.org/10.1055/s-2008-1045992.

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Biallowons, Ruth. "Höhentraining als Therapieoption bei Post- oder Long-Covid-Syndrom." Erfahrungsheilkunde 71, no. 05 (2022): 292–95. http://dx.doi.org/10.1055/a-1832-6297.

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ZusammenfassungDass Long Covid mit vordergründigem Erschöpfungssyndrom von einer Vielzahl von Ärzten als rein psychosomatisch eingestuft wird, wirft viele Erkrankte zurück und fördert die Entwicklung einer Chronifizierung. Patienten fühlen sich nicht ernst genommen und auch nicht zielführend untersucht. Da postvirale Erschöpfung dazu führt, dass selbst kleinste Alltagstätigkeiten nicht oder nur erschwert durchgeführt werden können, müssen die Patienten einer effizienten Therapie zugeführt werden. Das Höhentraining oder IHHT (Intervall-Hypoxie-Hyperoxie-Therapie) gilt als bewährte Methode zur S

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Casey, Darren P., Michael J. Joyner, Paul L. Claus, and Timothy B. Curry. "Vasoconstrictor responsiveness during hyperbaric hyperoxia in contracting human muscle." Journal of Applied Physiology 114, no. 2 (2013): 217–24. http://dx.doi.org/10.1152/japplphysiol.01197.2012.

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Large increases in systemic oxygen content cause substantial reductions in exercising forearm blood flow (FBF) due to increased vascular resistance. We hypothesized that 1) functional sympatholysis (blunting of sympathetic α-adrenergic vasoconstriction) would be attenuated during hyperoxic exercise and 2) α-adrenergic blockade would limit vasoconstriction during hyperoxia and increase FBF to levels observed under normoxic conditions. Nine male subjects (age 28 ± 1 yr) performed forearm exercise (20% of maximum) under normoxic and hyperoxic conditions. Studies were performed in a hyperbaric cha

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Hambraeus-Jonzon, K., L. Bindslev, C. Frostell, and G. Hedenstierna. "Individual lung blood flow during unilateral hypoxia: effects of inhaled nitric oxide." European Respiratory Journal 11, no. 3 (1998): 565–70. http://dx.doi.org/10.1183/09031936.98.11030565.

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We hypothesized that the diversion of blood away from a hypoxic lung to the opposite oxygenated lung can be enhanced by inhaling nitric oxide (NO) into the oxygenated lung. We measured individual lung blood flow when 50 ppm NO was selectively inhaled to: a hyperoxic lung during contralateral hypoxia; a normoxic lung during bilateral normoxia; and a hyperoxic lung during bilateral hyperoxia. Twenty two patients with healthy lungs were studied during intravenous anaesthesia. The lungs were separately and synchronously ventilated. The relative perfusion of each lung was assessed by the inert gas

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Petrache, Irina, Mary E. Choi, Leo E. Otterbein, et al. "Mitogen-activated protein kinase pathway mediates hyperoxia-induced apoptosis in cultured macrophage cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 277, no. 3 (1999): L589—L595. http://dx.doi.org/10.1152/ajplung.1999.277.3.l589.

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We have previously demonstrated that the lungs of mice can exhibit increased programmed cell death or apoptosis after hyperoxic exposure in vivo. In this report, we show that hyperoxic exposure in vitro can also induce apoptosis in cultured murine macrophage cells (RAW 264.7) as assessed by DNA-laddering, terminal deoxynucleotidyltransferase dUTP nick end-labeling, and nucleosomal assays. To further delineate the signaling pathway of hyperoxia-induced apoptosis in RAW 264.7 macrophages, we first show that hyperoxia can activate the mitogen-activated protein kinase (MAPK) pathway, the extracell

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Fang, Y., F. Gao та Z. Liu. "Angiotensin-converting enzyme 2 attenuates inflammatory response and oxidative stress in hyperoxic lung injury by regulating NF-κB and Nrf2 pathways". QJM: An International Journal of Medicine 112, № 12 (2019): 914–24. http://dx.doi.org/10.1093/qjmed/hcz206.

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Summary Objective To investigate the role of angiotensin-converting enzyme 2 (ACE2) in hyperoxic lung injury. Methods Adult mice were exposed to 95% O2 for 72 h to induce hyperoxic lung injury, and simultaneously treated with ACE2 agonist diminazene aceturate (DIZE) or inhibitor MLN-4760. ACE2 expression/activity in lung tissue and angiotensin (Ang)-(1–7)/Ang II in bronchoalveolar lavage fluid (BALF), and the severity of hyperoxic lung injury were evaluated. The levels of inflammatory factors in BALF and lung tissue and the expression levels of phospho-p65, p65 and IkBα were measured. Oxidativ

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Mak, Susanna, Zoltan Egri, Gemini Tanna, Rebecca Colman, and Gary E. Newton. "Vitamin C prevents hyperoxia-mediated vasoconstriction and impairment of endothelium-dependent vasodilation." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 6 (2002): H2414—H2421. http://dx.doi.org/10.1152/ajpheart.00947.2001.

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High arterial blood oxygen tension increases vascular resistance, possibly related to an interaction between reactive oxygen species and endothelium-derived vasoactive factors. Vitamin C is a potent antioxidant capable of reversing endothelial dysfunction due to increased oxidant stress. We tested the hypotheses that hyperoxic vasoconstriction would be prevented by vitamin C, and that acetylcholine-mediated vasodilation would be blunted by hyperoxia and restored by vitamin C. Venous occlusion strain gauge plethysmography was used to measure forearm blood flow (FBF) in 11 healthy subjects and 1

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Mhanna, Maroun J., Musa A. Haxhiu, Marwan A. Jaber, et al. "Hyperoxia impairs airway relaxation in immature rats via a cAMP-mediated mechanism." Journal of Applied Physiology 96, no. 5 (2004): 1854–60. http://dx.doi.org/10.1152/japplphysiol.01178.2002.

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Hyperoxic exposure enhances airway reactivity in newborn animals, possibly due to altered relaxation. We sought to define the role of prostaglandinand nitric oxide-mediated mechanisms in impaired airway relaxation induced by hyperoxic stress. We exposed 7-day-old rat pups to either room air or hyperoxia (>95% O2) for 7 days to assess airway relaxation and cAMP and cGMP production after electrical field stimulation (EFS). EFS-induced relaxation of preconstricted trachea was diminished in hyperoxic vs. normoxic animals ( P < 0.05). Indomethacin (a cyclooxygenase inhibitor) reduced EFS-indu

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Lodato, R. F., and A. Jubran. "Response time, autonomic mediation, and reversibility of hyperoxic bradycardia in conscious dogs." Journal of Applied Physiology 74, no. 2 (1993): 634–42. http://dx.doi.org/10.1152/jappl.1993.74.2.634.

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Normobaric hyperoxia decreases heart rate (HR) in humans and animals. This study explored the mechanisms of hyperoxic bradycardia by examining its response time, autonomic neural mediation, and reversibility in conscious dogs. Five trained mongrel dogs breathed from a mask as the inspired gas was alternated between air and O2 for multiple cycles, and continuous time series records of HR and oxyhemoglobin saturation were recorded on a digital computer and analyzed by the technique of ensemble averaging. Hyperoxia decreased HR by 9% (P < 0.001), but only gradually, requiring 5 min to reach st

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Seals, D. R., D. G. Johnson, and R. F. Fregosi. "Hyperoxia lowers sympathetic activity at rest but not during exercise in humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 5 (1991): R873—R878. http://dx.doi.org/10.1152/ajpregu.1991.260.5.r873.

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The primary aim of this study was to determine the influence of systemic hyperoxia on sympathetic nervous system behavior at rest and during submaximal exercise in humans. In seven healthy subjects (aged 19-31 yr) we measured postganglionic sympathetic nerve activity to skeletal muscle (MSNA) in the leg, antecubital venous norepinephrine concentrations, heart rate, and arterial blood pressure during normoxic rest (control) followed by 3- to 4-min periods of either hyperoxic (100% O2 breathing) rest, normoxic exercise (rhythmic handgrips at 50% of maximum force), or hyperoxic exercise. During e

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Sopi, Ramadan B., Musa A. Haxhiu, Richard J. Martin, Ismail A. Dreshaj, Suneel Kamath, and Syed I. A. Zaidi. "Disruption of NO-cGMP signaling by neonatal hyperoxia impairs relaxation of lung parenchyma." American Journal of Physiology-Lung Cellular and Molecular Physiology 293, no. 4 (2007): L1029—L1036. http://dx.doi.org/10.1152/ajplung.00182.2007.

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Exposure of immature lungs to hyperoxia for prolonged periods contributes to neonatal lung injury and airway hyperreactivity. We studied the role of disrupted nitric oxide-guanosine 3′,5′-cyclic monophosphate (NO-cGMP) signaling in impairing the relaxant responses of lung tissue from hyperoxia-exposed rat pups. Pups were exposed to ≥95% O2 or room air for 7 days starting from days 1, 5, or 14. The animals were killed, lungs were removed, and 1-mm-thick lung parenchymal strips were prepared. Lung parenchymal strips of room air or hyperoxic pups were preconstricted using bethanechol and then gra

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Houssière, Anne, Boutaina Najem, Nicolas Cuylits, Sophie Cuypers, Robert Naeije, and Philippe van de Borne. "Hyperoxia enhances metaboreflex sensitivity during static exercise in humans." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 1 (2006): H210—H215. http://dx.doi.org/10.1152/ajpheart.01168.2005.

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Peripheral chemoreflex inhibition with hyperoxia decreases sympathetic nerve traffic to muscle circulation [muscle sympathetic nerve activity (MSNA)]. Hyperoxia also decreases lactate production during exercise. However, hyperoxia markedly increases the activation of sensory endings in skeletal muscle in animal studies. We tested the hypothesis that hyperoxia increases the MSNA and mean blood pressure (MBP) responses to isometric exercise. The effects of breathing 21% and 100% oxygen at rest and during isometric handgrip at 30% of maximal voluntary contraction on MSNA, heart rate (HR), MBP, bl

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Yang, Yan, Xian Qin, Chuangang Han, et al. "Effect of different doses of dexmedetomidine on lung function and tissue cell apoptosis in a rat model of hyperoxic acute lung injury." Tropical Journal of Pharmaceutical Research 19, no. 5 (2020): 1093–98. http://dx.doi.org/10.4314/tjpr.v19i5.27.

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Purpose: To study the effect of different doses of dexmedetomidine on lung function and lung tissue cell apoptosis in a rat model of hyperoxic acute lung injury. Methods: Five groups of healthy male Sprague-Dawley rats were used: normal rats, untreated hyperoxic rats, and hyperoxic rats given 3 different doses of dexmedetomidine, with 20 rats in each group. The levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were determined usingenzyme-linked immunosorbent assay (ELISA). Parietal paraffin cuts were taken from the right upper lobe for measurement of apoptosis using in s

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SEPEHR, REYHANEH, SAID H. AUDI, SEPIDEH MALEKI, et al. "OPTICAL IMAGING OF LIPOPOLYSACCHARIDE-INDUCED OXIDATIVE STRESS IN ACUTE LUNG INJURY FROM HYPEROXIA AND SEPSIS." Journal of Innovative Optical Health Sciences 06, no. 03 (2013): 1350017. http://dx.doi.org/10.1142/s179354581350017x.

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Reactive oxygen species (ROS) have been implicated in the pathogenesis of many acute and chronic pulmonary disorders such as acute lung injury (ALI) in adults and bronchopulmonary dysplasia (BPD) in premature infants. Bacterial infection and oxygen toxicity, which result in pulmonary vascular endothelial injury, contribute to impaired vascular growth and alveolar simplification seen in the lungs of premature infants with BPD. Hyperoxia induces ALI, reduces cell proliferation, causes DNA damage and promotes cell death by causing mitochondrial dysfunction. The objective of this study was to use

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Moores, H. K., C. J. Beehler, M. E. Hanley, et al. "Xanthine oxidase promotes neutrophil sequestration but not injury in hyperoxic lungs." Journal of Applied Physiology 76, no. 2 (1994): 941–45. http://dx.doi.org/10.1152/jappl.1994.76.2.941.

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Neutrophil accumulation in alveolar spaces is a conspicuous finding in hyperoxia-exposed lungs. We hypothesized that xanthine oxidase (XO)-derived oxidants contribute to retention of neutrophils in hyperoxic lungs. Rats were subjected to normobaric hyperoxia (100% O2) for 48 h, and lungs were assessed for neutrophil sequestration (morphometry and lavage cell counts) and injury (lavage albumin levels and lung weights). In rats exposed to hyperoxia, we found increased (P < 0.05) lung neutrophil retention, lavage albumin levels, and lung weights compared with normoxia-exposed control rats. Sup

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Shnier, C. B., B. A. Cason, A. F. Horton, and R. F. Hickey. "Hyperoxemic reperfusion does not increase myocardial infarct size." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 4 (1991): H1307—H1312. http://dx.doi.org/10.1152/ajpheart.1991.260.4.h1307.

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We tested the hypothesis that arterial hyperoxia during myocardial reperfusion increases reperfusion injury and infarct size. The anterolateral marginal coronary artery of 35 anesthetized rabbits was occluded for 45 min, then reperfused for 3 h with either normoxic [arterial PO2 (PaO2) = 96.7 +/- 22.9 mmHg)] or hyperoxic (PaO2 = 554.8 +/- 61.7 mmHg) blood. In the hyperoxic group only, PaO2 was adjusted 10 s before the onset of reperfusion by raising inspired oxygen concentration to 100%. The area of infarction (AI) was defined by triphenyltetrazolium staining, and the area at risk (AR) by fluo

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Yamada, Mitsuhiro, Hiroshi Kubo, Seiichi Kobayashi, Kota Ishizawa та Hidetada Sasaki. "Interferon-γ: a key contributor to hyperoxia-induced lung injury in mice". American Journal of Physiology-Lung Cellular and Molecular Physiology 287, № 5 (2004): L1042—L1047. http://dx.doi.org/10.1152/ajplung.00155.2004.

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Hyperoxia-induced lung injury complicates the care of many critically ill patients who receive supplemental oxygen therapy. Hyperoxic injury to lung tissues is mediated by reactive oxygen species, inflammatory cell activation, and release of cytotoxic cytokines. IFN-γ is known to be induced in lungs exposed to high concentrations of oxygen; however, its contribution to hyperoxia-induced lung injury remains unclear. To determine whether IFN-γ contributes to hyperoxia-induced lung injury, we first used anti-mouse IFN-γ antibody to blockade IFN-γ activity. Administration of anti-mouse IFN-γ antib

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Chavez-Valdez, Raul, Ariel Mason, Ana R. Nunes, et al. "Effect of hyperoxic exposure during early development on neurotrophin expression in the carotid body and nucleus tractus solitarii." Journal of Applied Physiology 112, no. 10 (2012): 1762–72. http://dx.doi.org/10.1152/japplphysiol.01609.2011.

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Synaptic activity can modify expression of neurotrophins, which influence the development of neuronal circuits. In the newborn rat, early hyperoxia silences the synaptic activity and input from the carotid body, impairing the development and function of chemoreceptors. The purpose of this study was to determine whether early hyperoxic exposure, sufficient to induce hypoplasia of the carotid body and decrease the number of chemoafferents, would also modify neurotrophin expression within the nucleus tractus solitarii (nTS). Rat pups were exposed to hyperoxia (fraction of inspired oxygen 0.60) or

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Buckley, S., L. Barsky, K. Weinberg, and D. Warburton. "In vivo inosine protects alveolar epithelial type 2 cells against hyperoxia-induced DNA damage through MAP kinase signaling." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 3 (2005): L569—L575. http://dx.doi.org/10.1152/ajplung.00278.2004.

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Inosine, a naturally occurring purine with anti-inflammatory properties, was assessed as a possible modulator of hyperoxic damage to the pulmonary alveolar epithelium. Rats were treated with inosine, 200 mg/kg ip, twice daily during 48-h exposure to >90% oxygen. The alveolar epithelial type 2 cells (AEC2) were then isolated and cultured. AEC2 isolated from inosine-treated hyperoxic rats had less DNA damage and had increased antioxidant status compared with AEC2 from hyperoxic rats. Inosine treatment during hyperoxia also reduced the proportion of AEC2 in S and G2/M phases of the cell cycle

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Narasaraju, Telugu A., Nili Jin, Chintagari R. Narendranath, Zhongming Chen, Deming Gou, and Lin Liu. "Protein nitration in rat lungs during hyperoxia exposure: a possible role of myeloperoxidase." American Journal of Physiology-Lung Cellular and Molecular Physiology 285, no. 5 (2003): L1037—L1045. http://dx.doi.org/10.1152/ajplung.00008.2003.

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Several studies have suggested that exposure to hyperoxia causes lung injury through increased generation of reactive oxygen and nitrogen species. The present study was aimed to investigate the effects of hyperoxia exposure on protein nitration in lungs. Rats were exposed to hyperoxia (>95%) for 48, 60, and 72 h. Histopathological analysis showed a dramatic change in the severity of lung injury in terms of edema and hemorrhage between 48- and 60-h exposure times. Western blot for nitrotyrosine showed that several proteins with molecular masses of 29-66 kDa were nitrated in hyperoxic lung ti

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Richter, Jute, Jaan Toelen, Jeroen Vanoirbeek, et al. "Functional assessment of hyperoxia-induced lung injury after preterm birth in the rabbit." American Journal of Physiology-Lung Cellular and Molecular Physiology 306, no. 3 (2014): L277—L283. http://dx.doi.org/10.1152/ajplung.00315.2013.

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The objective of this study was to document early neonatal (7 days) pulmonary outcome in the rabbit model for preterm birth and hyperoxia-induced lung injury. Preterm pups were delivered at 28 days (term = 31 days; early saccular phase of lung development) by cesarean section, housed in an incubator, and gavage fed for 7 days. Pups were divided into the following groups: 1) normoxia (21% O2; normoxia group) and 2) and hyperoxia (>95% O2; hyperoxia group). Controls were pups born at term who were housed in normoxic conditions (control group). Outcome measures were survival, pulmonary functio

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Nagano, Nobuhiko, Kosuke Tanaka, Junichi Ozawa, et al. "Attenuation of Hyperoxic Lung Injury in Newborn Thioredoxin-1-Overexpressing Mice through the Suppression of Proinflammatory Cytokine mRNA Expression." Biomedicines 8, no. 3 (2020): 66. http://dx.doi.org/10.3390/biomedicines8030066.

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The role of thioredoxin-1 (TRX), a small redox-active protein with antioxidant effects, during hyperoxic lung injury in newborns remains undetermined. We investigated TRX impact on hyperoxic lung injury in newborn TRX transgenic (TRX-Tg) and wildtype (WT) mice exposed to 21% or 95% O2 for four days, after which some mice were allowed to recover in room air for up to 14 days. Lung morphology was assessed by hematoxylin/eosin and elastin staining, as well as immunostaining for macrophages. The gene expression levels of proinflammatory cytokines were evaluated using quantitative real-time polymer

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Hughson, Richard L., and John M. Kowalchuk. "Kinetics of Oxygen Uptake for Submaximal Exercise in Hyperoxia, Normoxia, and Hypoxia." Canadian Journal of Applied Physiology 20, no. 2 (1995): 198–210. http://dx.doi.org/10.1139/h95-014.

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This study evaluated the dynamic response of [Formula: see text] in 6 healthy men at the onset and end of submaximal step changes in work rate during a pseudorandom binary sequence (PRBS) exercise test and during ramp incremental exercise to exhaustion while breathing three different gas mixtures. The fractional concentrations of inspired O2 were 0.14, 0.21, and 0.70 for the hypoxic, normoxic, and hyperoxic tests, respectively. Both maximal [Formula: see text] and work rate was significantly reduced in hypoxic tests compared to normoxic and hyperoxic tests. Maximal work rate was greater in hyp

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