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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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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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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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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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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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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 chamber where fraction of inspired oxygen (FiO2) was 0.21, 2) Hyperoxic group; rats were placed in hyperoxic chamber (FiO2>0.8) using an oxygen flow of 1.5 Litre/min, 3) Hyperoxia-CAF group; rats exposed to hyperoxia and received a single intra-peritoneal injection of 20 mg/kg caffeine just prior to exposure, and 4) Hyperoxia-NAC group; rats exposed to hyperoxia and received a single intra-peritoneal injection of 150 mg/kg N-acetylcysteine just prior to exposure. 48 hours after exposure, lung specimens were processed for histological and immunohistochemical study using caspase-3, cluster of differentiation-68-antibody (CD68) and interleukin-1-beta (IL-1β). Results: Neonatal hyperoxia led to severe impairment in lung architecture, with a highly significant increase in alveolar macrophages. Also, caspase and IL-1β immune-reaction were increased significantly as compared to control group. Caffeine could improve the histolopathological picture of hyperoxic acute lung injury, and also could decrease alveolar macrophage count and IL-1β immune-reaction better than N-acetylcysteine. Conclusion: Caffeine is more effective than N-acetylcysteine in prophylaxis against hyperoxic acute lung injury in neonates.
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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 (mtALDH-A549) decreased from 25.3 to 6.5%, 50.5 to 9.1%, and 52.4 to 15.1% after 24-, 48-, and 72-h hyperoxic exposure, respectively. The levels of intracellular and mitochondria-derived reactive oxygen species (ROS) in mtALDH-A549 cells after hyperoxic exposure were significantly lowered compared with Neo-A549 cells. mtALDH overexpression significantly stimulated extracellular signal-regulated kinase (ERK) phosphorylation under normoxic and hyperoxic conditions. Inhibition of ERK phosphorylation partially eliminated the protective effect of mtALDH in hyperoxia-induced cell death, suggesting ERK activation by mtALDH conferred cellular resistance to hyperoxia. mtALDH overexpression augmented Akt phosphorylation and maintained the total Akt level in mtALDH-A549 cells under normoxic and hyperoxic conditions. Inhibition of phosphatidylinositol 3-kinase (PI3K) activation by LY294002 in mtALDH-A549 cells significantly increased necrotic cell death after hyperoxic exposure, indicating that PI3K-Akt activation by mtALDH played an important role in cell survival after hyperoxia. Taken together, these data demonstrate that mtALDH overexpression attenuates hyperoxia-induced cell death in lung epithelial cells through reduction of ROS, activation of ERK/MAPK, and PI3K-Akt cell survival signaling pathways.
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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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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 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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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. TGF-β1 was protective over a concentration range similar to that in BAL of inosine-treated hyperoxic animals (50–5,000 pg/ml). TGF-β1 also augmented hyperoxia-induced DNA repair activity and cell migration, stimulated autocrine secretion of fibronectin, accelerated closure of a monolayer scratch wound, and restored hyperoxia-depleted VEGF secretion by AEC2 to normoxic levels. The TGF-β receptor type I activin-like kinase-4, -5, and -7 inhibitor peptide SB-505124 abolished the protective effect of TGF-β on hyperoxic DNA damage and increased TdT-mediated dUTP nick end labeling in normoxic cells. These data suggest that endogenous TGF-β-mediated Smad signaling is required for AEC2 homeostasis in vitro, while exogenous TGF-β1 treatment of hyperoxia-damaged AEC2 results in a cell that is equipped to survive, repair, migrate, secrete matrix, and induce new blood vessel formation more efficiently than AEC2 primed by hyperoxia alone.
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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 assumption by demonstrating that O2 has central effects on the brain stem respiratory centers and several effects on neurons in respiratory control areas; these need to be considered whenever hyperoxia is used. This mini-review summarizes the long-recognized, but seldom acknowledged, paradox of respiratory control known as hyperoxic hyperventilation. Several proposed mechanisms are discussed, including the recent hypothesis that hyperoxic hyperventilation is initiated by increased production of ROS during hyperoxia, which directly stimulates central CO2 chemoreceptors in the solitary complex. Hyperoxic hyperventilation may provide clues into the fundamental role of redox signaling and ROS in central control of breathing; moreover, oxidative stress may play a role in respiratory control dysfunction. The practical implications of brain stem O2 and ROS sensitivity are also considered relative to the present uses of hyperoxia in respiratory control research in humans, animals, and brain stem tissues. Recommendations for future research are also proposed.
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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 processed for detection of iNOS by immunohistochemistry and Western blotting analysis. The same experiments were repeated in animals exposed to hyperoxia for 72 h after they were infused with l-arginine. We used rats that were injected intraperitoneally with Escherichia coli lipopolysaccharide to induce septic shock as a positive control group. Hyperoxia and septic shock induced expression of iNOS in the lung. However, ENO was elevated only in septic shock rats but was normal in the hyperoxic group. Exogenous infusion of l-arginine after hyperoxia did not increase ENO. To exclude the possibility that in the hyperoxic group NO was scavenged by oxygen radicals to form peroxynitrite, lungs were studied by immunohistochemistry for the detection of nitrotyrosine. Nitrotyrosine was found in septic shock animals but not in the hyperoxic group, further suggesting that NO is not synthesized in rats exposed to hyperoxia. We conclude that hyperoxia induces iNOS expression in the lung without an increase in NO concentration in the exhaled air.
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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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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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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, animals were maintained in room air until early adulthood at postnatal day 56 ( P56d) or middle age (10 mo; P10mo). Pups were assessed for glomerular maturity and renal corpuscle cross-sectional area at P7d (control n = 14; hyperoxic n = 14). Nephron number and renal corpuscle size were determined stereologically at P56d (control n = 14; hyperoxic n = 14) and P10mo (control n = 10; hyperoxic n = 10). At P7d, there was no effect of hyperoxia on glomerular size or maturity. In early adulthood ( P56d), body weights, relative kidney weights and volumes, and nephron number were not different between groups, but the renal corpuscles were significantly enlarged. This was no longer evident at P10mo, with relative kidney weights and volumes, nephron number, and renal corpuscle size not different between groups. Furthermore, hyperoxia exposure did not significantly accelerate glomerulosclerosis in middle age. Hence, our findings show no overt long-term deleterious effects of early life hyperoxia on glomerular structure.
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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 MAS receptor was previously shown to have protective pulmonary responses. However, the effect of MAS receptor activation on surfactant proteins in hyperoxic conditions has not been tested. Objective: To determine the effects of hyperoxia with or without MAS receptor activation on Surfactant proteins. Methods: Human epithelial cell line A549 and human primary alveolar epithelial cells (AECs) were cultured to sub-confluence (60-75%) and treated with hyperoxia (95% oxygen) and normoxia (21% oxygen) for 72 hours with or without the MAS receptor agonist (AVE0991) in serum-free F-12 nutrient media. Cells were lysed and cell lysates were collected for western blot. The statistical analysis was done using Student-Newman-Keuls Multiple comparison test. Results: Surfactant protein concentration increased in AVE treated group under the hyperoxic condition when compared to the control group in both A549 cells and human primary AECs. Surfactant protein was in higher concentration in AVE0991 treated cells in both hyperoxic and normoxic conditions when compared to the non-treated control group. Conclusions: MAS receptor activation via AVE0991 causes an increase in Surfactant protein concentration in both hyperoxic and normoxic conditions. As per our experiments, hyperoxic conditions decrease the production of surfactant protein when compared to normoxic conditions. These results may reveal a novel potential drug for BPD treatment and decrease its severity.
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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 administered the following gas mixtures for 60 h: 98% oxygen (hyperoxia), 2% nitrogen; 98% oxygen (hyperoxia), 2% hydrogen; 98% balanced air (normoxia), 2% nitrogen; and 98% balanced air (normoxia), 2% hydrogen. We examined lung function by blood gas analysis, extent of lung injury, and expression of HO-1. We also investigated the role of NF-E2-related factor (Nrf) 2, which regulates HO-1 expression, by examining the expression of Nrf2-dependent genes and the ability of hydrogen to reduce hyperoxic lung injury in Nrf2-deficient mice. Hydrogen treatment during exposure to hyperoxia significantly improved blood oxygenation, reduced inflammatory events, and induced HO-1 expression. Hydrogen did not mitigate hyperoxic lung injury or induce HO-1 in Nrf2-deficient mice. These findings indicate that hydrogen gas can ameliorate hyperoxic lung injury through induction of Nrf2-dependent genes, such as HO-1. The findings suggest a potentially novel and applicable solution to hyperoxic lung injury and provide new insight into the molecular mechanisms and actions of hydrogen.
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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 >100 mmHg and extreme hyperoxia > 300 mmHg (a subset of hyperoxia). We defined serious injuries as those with an Abbreviated Injury Score (AIS) of 3 or greater. We defined a probable moderate traumatic brain injury of those with an AIS of 3 or greater for the head region and at least one Glasgow Coma Scale at 8 or less. Results Our initial search yielded 28,222 casualties, of which 10,969 had at least one ABG available. Within the 10,969, the proportion of casualties experiencing hyperoxia in this population was 20.6% (2,269) with a subset of 4.1% (452) meeting criteria for extreme hyperoxia. Among those with hyperoxia, the median age was 25 years (IQR 21–30), most were male (96.8%), most frequently US forces (41.4%), injured in Afghanistan (68.3%), injured by explosive (61.1%), with moderate injury scores (median 17, IQR 10–26), and most (93.8%) survived to hospital discharge. A total of 17.8% (1,954) of the casualties underwent endotracheal intubation: 27.5% (538 of 1,954) prior to emergency department (ED) arrival and 72.5% (1,416 of 1,954) within the ED. Among those intubated in the prehospital setting, upon ED arrival 35.1% (189) were hyperoxic, and a subset of 5.6% (30) that were extremely hyperoxic. Among those intubated in the ED, 35.4% (502) were hyperoxic, 7.9% (112) were extremely hyperoxic. Within the 1,277 with a probable TBI, 44.2% (565) experienced hyperoxia and 9.5% (122) met criteria for extreme hyperoxia. Conclusions In our dataset, more than 1 in 5 casualties overall had documented hyperoxia on ABG measurement, 1 in 3 intubated casualties, and almost 1 in 2 TBI casualties. With limited oxygen supplies in theater and logistical challenges with oxygen resupply, efforts to avoid unnecessary oxygen supplementation may have material impact on preserving this scarce resource and avoid potential detrimental clinical effects from supraphysiologic oxygen concentrations.
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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 for in vitro study. Results Formononetin pretreatment notably attenuated hyperoxia-induced elevating pulmonary water content, upregulation of proinflammatory cytokine levels and increasing infiltration of neutrophil in the lung. Western blot analyses showed that Formononetin enhanced the expression of nuclear factor erythroid-2-related factor 2 (Nrf2) which is a key transcription factor regulating the expression of heme oxygenase-1 (HO-1). Formononetin increased HO-1 expression and activity compared with vehicle-treated animals. Moreover, Formononetin reversed hyperoxia-caused the reduction of M2 macrophage polarization. However, pretreatment of a HO-1 inhibitor reduced the protective effect of Formononetin on hyperoxic ALI. Cell study showed that the Formononetin-induced upregulation of HO-1 was abolished when the Nrf2 was silenced. Conclusions Formononetin pretreatment reduces hyperoxia-induced ALI via Nrf2/HO-1-mediated antioxidant and anti-inflammatory effects.
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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 stimulation were measured in vitro in normoxia- and hyperoxia-exposed tracheal cylinders. Hyperoxia caused a 1.1- to 2.6-fold increase in steady-state lung beta-PPT mRNA and a 50 and 32% increase in SP levels of lung and trachea, respectively. In response to cholinergic stimulation, maximal contractile force (Emax) of hyperoxia exposed tracheal muscle was significantly higher than for normoxic controls. Addition of the SP (NK1) receptor blocker CP-99994 (10 microM) decreased sensitivity to electrical field stimulation in both hyperoxic and normoxic trachea without a significant decline in Emax. These data provide evidence for both increased SP production and enhanced maximal contractile responses of hyperoxia-exposed neonatal trachea to cholinergic stimulation. The tachykinin peptide SP does not, however, appear to play a major role in the enhanced airway reactivity associated with hyperoxic lung injury during early postnatal life.
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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 rat pups were exposed to ≥95% oxygen or room air for 7 days and administered daily tyrosine kinase inhibitor K-252a (50 μg·kg−1·day−1 ip) to block BDNF-TrkB signaling or vehicle. Lungs were removed for HPLC measurement of ACh or for in vitro force measurement of lung parenchymal strips. ACh content doubled in hyperoxic compared with room air-exposed lungs. K-252a treatment of hyperoxic pups restored ACh content to room air levels. Hyperoxia increased contraction and impaired relaxation of lung strips in response to incremental electrical field stimulation. K-252a administration to hyperoxic pups reversed this increase in contraction and decrease in relaxation. K-252a or TrkB-Fc was used to block the effect of exogenous BDNF in vitro. Both K-252a and TrkB-Fc blocked the effects of exogenous BDNF. Hyperoxia decreased cAMP and cGMP levels in lung strips, and blockade of BDNF-TrkB signaling restored cAMP but not cGMP to control levels. Therefore, hyperoxia-induced increase in activity of BDNF-TrkB receptor signaling appears to play a critical role in enhancing cholinergically mediated contractile responses of lung parenchyma.
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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 therapeutic approaches in the clinic. Changes in oxygen availability can be detrimental to cellular function and contribute to oxidative damage. Here, we sought to determine the effect of oxygen on mitochondria in human fetal airway smooth muscle cells exposed to either 5% O2, 21% O2, 40% O2, or cycles of 5% and 40% O2 (intermittent hypoxia-hyperoxia). Reactive oxygen species production, altered mitochondrial morphology, and changes in mitochondrial respiration were assessed in the context of the antioxidant N-acetylcysteine. Our findings show developing airway smooth muscle is differentially responsive to hypoxic, hyperoxic, or intermittent hypoxic-hyperoxic exposure in terms of mitochondrial structure and function. Cycling O2 decreased mitochondrial branching and branch length similar to hypoxia and hyperoxia in the presence of antioxidants. Additionally, hypoxia decreased overall mitochondrial respiration while the addition of antioxidants increased respiration in normoxic and O2-cycling conditions. These studies show the necessity of balancing oxidative damage and antioxidant defense systems in the developing airway.
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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 reperfusion: the hyperoxic group (PaO2 > 200 mmHg) and the nonhyperoxic group (PaO2 < 200 mmHg). The primary endpoint was arterial lactatemia 15 min after graft revascularization. Secondary endpoints included postoperative clinical outcomes and laboratory data. Results: A total of 222 liver transplant recipients were included. Arterial lactatemia after graft revascularization was significantly higher in the hyperoxic group (6.03 ± 4 mmol/L) than in the nonhyperoxic group (4.81 ± 2 mmol/L), p < 0.01. The postoperative hepatic cytolysis peak, duration of mechanical ventilation and duration of ileus were significantly increased in the hyperoxic group. Conclusions: In the hyperoxic group, the arterial lactatemia, the hepatic cytolysis peak, the mechanical ventilation and the postoperative ileus were higher than in the nonhyperoxic group, suggesting that hyperoxia worsens short-term outcomes and could lead to increase ischemia–reperfusion injury after liver transplantation. A multicenter prospective study should be performed to confirm these results.
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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 infarct volumes, regional cerebral blood flow (rCBF) using laser Doppler flowmetry, and severity of BBB damage (assessed by quantifying Evan’s Blue dye (EB) leakage after one hour of reperfusion) were compared between groups. Results: Physiological parameters were similar in hyperoxic and control groups, except for paO2, which was expectedly higher in the hyperoxic group (pO2 484 mm Hg) as compared to controls (pO2 118 mm Hg). Mean rCBF dropped to 25% after onset of ischemia and recovered to 75–90% after arterial unocclusion, indicating successful reperfusion. Mean total (right hemispheric) infarct volume was 65 mm 3 in the hyperoxia group and 209 mm 3 in controls, p<0.001. The reduction in infarct volume was mostly in the cortex, where mean infarct volume was 11 mm 3 in hyperoxic rats and 129 mm 3 in controls (p<0.001). Mean striatal infarct volume was 54 mm 3 in hyperoxic rats and 80 mm 3 in controls (p<0.06). Mean total EB leak was 1592 ng/g in hyperoxic and 3955 ng/g in control rats (p<0.02), suggesting reduced BBB damage in hyperoxia. However, BBB damage and EB leak are likely related to infarct volume; after normalising for infarct volume, mean EB leak was 17 ng/mm3 in the hyperoxia group and 14 ng/mm3 in controls (p=0.5). Conclusion: Total and cortical infarct volumes can be significantly reduced with normobaric hyperoxia during transient cerebral ischemia and reperfusion. Hyperoxia does not decrease blood flow to ischemic brain, and its benefit in reducing infarct volume may outweigh any potential damage from BBB damage.
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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 mitigate HALI by ameliorating HMGB1-compromised macrophage function in phagocytosis by attenuating hyperoxia-induced extracellular HMGB1 accumulation. Our results indicated that SFN, which has been shown to attenute HALI in mice exposed to hyperoxia, dose-dependently restored hyperoxia-compromised macrophage function in phagocytosis (75.9 ± 3.5% in 0.33 µM SFN versus 50.7 ± 1.8% in dimethyl sulfoxide (DMSO) control, p < 0.05) by reducing oxidative stress and HMGB1 release from cultured macrophages (47.7 ± 14.7% in 0.33 µM SFN versus 93.1 ± 14.6% in DMSO control, p < 0.05). Previously, we have shown that AA enhances hyperoxic macrophage functions by reducing hyperoxia-induced HMGB1 release. Using a mouse model of HALI, we determined the effects of AA on hyperoxia-induced inflammatory lung injury. The i.p. administration of 50 mg/kg of AA to mice exposed to 72 h of ≥98% O2 significantly decreased hyperoxia-induced oxidative and nitrosative stress in mouse lungs. There was a significant decrease in the levels of airway HMGB1 (43.3 ± 12.2% in 50 mg/kg AA versus 96.7 ± 9.39% in hyperoxic control, p < 0.05), leukocyte infiltration (60.39 ± 4.137% leukocytes numbers in 50 mg/kg AA versus 100 ± 5.82% in hyperoxic control, p < 0.05) and improved lung integrity in mice treated with AA. Our study is the first to report that the dietary antioxidants, ascorbic acid and sulforaphane, ameliorate HALI and attenuate hyperoxia-induced macrophage dysfunction through an HMGB1-mediated pathway. Thus, dietary antioxidants could be used as potential treatments for oxidative-stress-induced acute inflammatory lung injury in patients receiving mechanical ventilation.
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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) higher performance of the repeated Wingate test aft er inhaling concentrated oxygen in comparison with the placebo at both low and higher altitudes. Inhalation of concentrated oxygen aff ects performance to a greater extent at the higher altitude compared to that of the low altitude.
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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 Steigerung der Leistungsfähigkeit im Leistungssport und wird in der Praxis beim Post-Covid-Syndrom eingesetzt mit dem Ziel, die individuelle Regulationsfähigkeit wiederherzustellen. Der Beitrag zeigt die Praxiserfahrung der IHHT-Anwendung in den letzten 2 Jahren in der Praxis Biallomed in Düsseldorf.
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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 chamber at 1 atmosphere absolute (ATA; sea level) while breathing 21% O2 and at 2.82 ATA while breathing 100% O2 (estimated change in arterial O2 content ∼6 ml O2/100 ml). FBF (ml/min) was measured using Doppler ultrasound. Forearm vascular conductance (FVC) was calculated from FBF and blood pressure (arterial catheter). Vasoconstrictor responsiveness was determined using intra-arterial tyramine. FBF and FVC were substantially lower during hyperoxic exercise than normoxic exercise (∼20–25%; P < 0.01). At rest, vasoconstriction to tyramine (% decrease from pretyramine values) did not differ between normoxia and hyperoxia ( P > 0.05). During exercise, vasoconstrictor responsiveness was slightly greater during hyperoxia than normoxia (−22 ± 3 vs. −17 ± 2%; P < 0.05). However, during α-adrenergic blockade, hyperoxic exercise FBF and FVC remained lower than during normoxia ( P < 0.01). Therefore, our data suggest that although the vasoconstrictor responsiveness during hyperoxic exercise was slightly greater, it likely does not explain the majority of the large reductions in FBF and FVC (∼20–25%) during hyperbaric hyperoxic exercise.
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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 elimination technique. Unilateral hypoxic (inspiratory oxygen fraction (FI,O2) 0.05) ventilation during contralateral hyperoxia reduced the perfusion of the hypoxic lung from a mean (SD) of 47 (9)% of cardiac output (Q'), to 30 (7)% (p<0.001) of Q'. NO inhalation to the hyperoxic lung increased its blood flow from 70 (7)% to 75 (6)% (p<0.05) of Q', and reduced the blood flow to the hypoxic lung to 25 (6)% (p<0.05). Unilateral NO inhalation during bilateral normoxia or hyperoxia had no effect on pulmonary blood flow distribution. Nitric oxide inhalation to a hyperoxic lung increases the perfusion to this lung by redistribution of blood flow if the opposite lung is hypoxic.
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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 extracellular signal-regulated kinases (ERKs) p42/p44, in a time-dependent manner as assessed by increased phosphorylation of ERK1/ERK2 by Western blot analyses. Neither the c-Jun NH2-terminal kinase/stress-activated protein kinase nor the p38 MAPK was activated by hyperoxia in these cells. Chemical or genetic inhibition of the ERK p42/p44 MAPK pathway by PD-98059, a selective inhibitor of MAPK kinase, and dominant negative mutants of ERK, respectively, attenuated hyperoxia-induced apoptosis as assessed by DNA laddering and nucleosomal ELISAs. Taken together, our data suggest that hyperoxia can induce apoptosis in cultured murine macrophages and that the MAPK pathway mediates hyperoxia-induced apoptosis.
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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. Oxidative parameter and antioxidant enzyme levels in lung tissue were measured to assess oxidative stress. Finally, the expression levels of nuclear factor-erythroid-2-related factor (Nrf2), NAD(P)H quinine oxidoreductase 1 (NQO1) and heme oxygenase-1 (HO-1) were measured using Western blotting. Results Hyperoxia treatment significantly decreased lung ACE2 expression/activity and increased the Ang II/Ang-(1–7) ratio, while co-treatment with hyperoxia and DIZE significantly increased lung ACE2 expression/activity and decreased the Ang II/Ang-(1–7) ratio. By contrast, co-treatment with hyperoxia and MLN-4760 significantly decreased lung ACE2 expression/activity and increased the Ang II/Ang-(1–7) ratio. Hyperoxia treatment induced significant lung injury, inflammatory response and oxidative stress, which were attenuated by DIZE but aggravated by MLN-4760. The NF-κB pathways were activated by hyperoxia and MLN-4760 but inhibited by DIZE. The Nrf2 pathway and its downstream proteins NQO1 and HO-1 were activated by DIZE but inhibited by MLN-4760. Conclusion Activation of ACE2 can reduce the severity of hyperoxic lung injury by inhibiting inflammatory response and oxidative stress. ACE2 can inhibit the NF-κB pathway and activate the Nrf2/HO-1/NQO1 pathway, which may be involved in the underlying mechanism.
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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 15 congestive heart failure (CHF) patients, a population characterized by endothelial dysfunction and oxidative stress. The effect of hyperoxia on FBF and derived forearm vascular resistance (FVR) at rest and in response to intra-arterial acetylcholine was recorded. In both healthy subjects and CHF patients, hyperoxia-mediated increases in basal FVR were prevented by the coinfusion of vitamin C. In healthy subjects, hyperoxia impaired the acetylcholine-mediated increase in FBF, an effect also prevented by vitamin C. In contrast, hyperoxia had no effect on verapamil-mediated increases in FBF. In CHF patients, hyperoxia did not affect FBF responses to acetylcholine or verapamil. The addition of vitamin C during hyperoxia augmented FBF responses to acetylcholine. These results suggest that hyperoxic vasoconstriction is mediated by oxidative stress. Moreover, hyperoxia impairs acetylcholine-mediated vasodilation in the setting of intact endothelial function. These effects of hyperoxia are prevented by vitamin C, providing evidence that hyperoxia-derived free radicals impair the activity of endothelium-derived vasoactive factors.
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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-induced airway relaxation in tracheae from normoxic ( P < 0.05), but not hyperoxic, rat pups; however, in the presence of NG-nitro-l-arginine methyl ester (a nitric oxide synthase inhibitor) EFS-induced airway relaxation was similarly decreased in tracheae from both normoxic and hyperoxic animals. After EFS, the increase from baseline in the production of cAMP was significantly higher in tracheae from normoxic than hyperoxic rat pups, and this was accompanied by greater prostaglandin E2 release only in the normoxic group. cGMP production after EFS stimulation did not differ between normoxic and hyperoxic groups. We conclude that hyperoxia impairs airway relaxation in immature animals via a mechanism primarily involving the prostaglandin-cAMP signaling pathway with an impairment of prostaglandin E2 release and cAMP accumulation.
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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 steady state. This delay was much longer than the time required for hyperoxic respiratory depression (10–20 s), a response known to be mediated by chemoreceptor reflexes. The bradycardia was sustained for > or = 30 min. On return to normoxia, HR gradually returned toward, but failed to reach, the baseline HR, suggesting incomplete reversibility of the response. However, in control experiments without hyperoxic challenge, HR showed a slow continuous downward trend that was sufficient to account for the apparent incomplete reversibility of hyperoxic bradycardia. Hyperoxic bradycardia was unaffected by beta-adrenergic blockade but was completely prevented by muscarinic cholinergic blockade. We conclude that 1) hyperoxia-induced bradycardia in conscious dogs is mediated by efferents of the vagus nerve; 2) its afferent pathway remains unknown, but its long response time suggests mechanisms other than chemoreceptor reflexes or other known neural reflexes; and 3) it is completely reversible.
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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 exercise, isocapnia was maintained by adding CO2 to the inspirate as necessary. At rest, hyperoxia lowered MSNA burst frequency (12-42%) and total activity (6-42%) in all subjects; the average reductions were 25 and 23%, respectively (P less than 0.05 vs. control). Heart rate also decreased during hyperoxia (6 +/- 1 beats/min, P less than 0.05), but arterial blood pressure was not affected. During hyperoxic compared with normoxic exercise, there were no differences in the magnitudes of the increases in MSNA burst frequency or total activity, plasma norepinephrine concentrations, or mean arterial blood pressure. In contrast, the increase in heart rate during hyperoxic exercise (13 +/- 2 beats/min) was less than the increase during normoxic exercise (20 +/- 2 beats/min; P less than 0.05). We conclude that, in healthy humans, systemic hyperoxia 1) lowers efferent sympathetic nerve activity to skeletal muscle under resting conditions without altering venous norepinephrine concentrations and 2) has no obvious modulatory effect on the nonactive muscle sympathetic nerve adjustments to rhythmic exercise.
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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 graded electrical field stimulation (EFS) was applied to induce relaxation. EFS-induced relaxation of lung parenchymal strips was greater at 7 and 12 days than at 21 days in room air-exposed rat pups. Hyperoxic exposure significantly reduced relaxation at 7 and 12 days but not 21 days compared with room air exposure. NO synthase blockade with Nω-nitro-l-arginine methyl ester diminished relaxant responses in room air but not in hyperoxic pups at 12 days. After incubation with supplemental l-arginine, the relaxation response of hyperoxic strips was restored. cGMP, a key mediator of the NO signaling pathway, also decreased in strips from hyperoxic vs. room air pups and cGMP levels were restored after incubation with supplemental l-arginine. In addition, arginase activity was significantly increased in hyperoxic lung parenchymal strips compared with room air lung parenchymal strips. These data demonstrate disruption of NO-cGMP signaling in neonatal rat pups exposed to hyperoxia and show that bioavailability of the substrate l-arginine is implicated in the predisposition of this model to airway hyperreactivity.
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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, blood lactate (BL), and arterial O2 saturation (SaO2) were determined in 12 healthy men. The isometric handgrips were followed by 3 min of postexercise circulatory arrest (PE-CA) to allow metaboreflex activation in the absence of other reflex mechanisms. Hyperoxia lowered resting MSNA, HR, MBP, and BL but increased SaO2 compared with normoxia (all P < 0.05). MSNA and MBP increased more when exercise was performed in hyperoxia than in normoxia (MSNA: hyperoxic exercise, 255 ± 100% vs. normoxic exercise, 211 ± 80%, P = 0.04; and MBP: hyperoxic exercise, 33 ± 9 mmHg vs. normoxic exercise, 26 ± 10 mmHg, P = 0.03). During PE-CA, MSNA and MBP remained elevated (both P < 0.05) and to a larger extent during hyperoxia than normoxia ( P < 0.05). Hyperoxia enhances the sympathetic and blood pressure (BP) reactivity to metaboreflex activation. This is due to an increase in metaboreflex sensitivity by hyperoxia that overrules the sympathoinhibitory and BP lowering effects of chemoreflex inhibition. This occurs despite a reduced lactic acid production.
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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 situ terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and the apoptosis index was calculated.
 Results: At 24 and 48 h, the levels of IL-6 and TNF-α in the hyperoxia model group were significantly higher than those in the normal control group, and their levels in the middle- and high-dose groups were markedly lowered, relative to untreated hyperoxia rats (p < 0.05). Apoptosis index in the hyperoxia model rats significantly increased, relative to normal rats (p < 0.05). The apoptosis index in the mediumand high-dose groups decreased significantly (p < 0.05).
 Conclusion: Dexmedetomidine inhibits inflammatory responses caused by high concentration of oxygen inhalation, minimizes lung injury, improves lung function and inhibits lung apoptosis.
 Keywords: Dexmedetomidine, Hyperoxia, Acute lung injury, Lung function, Apoptosis
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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 an optical imaging technique to evaluate the variations in fluorescence intensities of the auto-fluorescent mitochondrial metabolic coenzymes, NADH and FAD in four different groups of rats. The ratio of these fluorescence signals (NADH/FAD), referred to as NADH redox ratio (NADH RR) has been used as an indicator of tissue metabolism in injuries. Here, we investigated whether the changes in metabolic state can be used as a marker of oxidative stress caused by hyperoxia and bacterial lipopolysaccharide (LPS) exposure in neonatal rat lungs. We examined the tissue redox states of lungs from four groups of rat pups: normoxic (21% O2 ) pups, hyperoxic (90% O2 ) pups, pups treated with LPS (normoxic + LPS), and pups treated with LPS and hyperoxia (hyperoxic + LPS). Our results show that hyperoxia oxidized the respiratory chain as reflected by a ~ 31% decrease in lung tissue NADH RR as compared to that for normoxic lungs. LPS treatment alone or with hyperoxia had no significant effect on lung tissue NADH RR as compared to that for normoxic or hyperoxic lungs, respectively. Thus, NADH RR serves as a quantitative marker of oxidative stress level in lung injury caused by two clinically important conditions: hyperoxia and LPS exposure.
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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. Suppression of XO activity by pretreatment with allopurinol decreased (P < 0.05) lung neutrophil retention but increased (P < 0.05) lavage albumin concentrations and lung weights in hyperoxic rats. Allopurinol treatment had no effect (P > 0.05) on the numbers of macrophages or lymphocytes recoverable by lung lavage. Depletion of XO activity by an independent method, tungsten feeding, also decreased (P < 0.05) lung lavage neutrophil counts and increased (P < 0.05) lavage albumin concentrations. We conclude that XO may be involved in lung neutrophil retention but not lung injury during exposure to hyperoxia.
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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 fluorescent microspheres. These areas were measured by planimetry. Heart rates and blood pressures did not differ between the two groups during occlusion or reperfusion. Infarct size (AI/AR) was 49.1 +/- 16.5% in the normoxic group (n = 17) and 40.8 +/- 16.1% in the hyperoxic group (n = 18). From these data, 90% confidence limits establish that the maximal true increase in AI/AR caused by hyperoxia would be 0%-1%. Hyperoxic reperfusion of ischemic myocardium compared with normoxic reperfusion does not significantly increase myocardial infarct size.
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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.
Full textAbstract:
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 antibody inhibited hyperoxia-induced increases in pulmonary alveolar permeability and neutrophil migration into lung air spaces. To confirm that IFN-γ contributes to hyperoxic lung injury, we then simultaneously exposed IFN-γ-deficient (IFN-γ−/−) mice and wild-type mice to hyperoxia. In the early phase of hyperoxia, permeability changes and neutrophil migration were significantly reduced in IFN-γ−/− mice compared with wild-type mice, although the differences in permeability changes and neutrophil migration between IFN-γ−/− mice and wild-type mice were not significant in the late phase of hyperoxia. The concentrations of IL-12 and IL-18, two cytokines that play a role in IFN-γ induction, significantly increased in bronchoalveolar lavage fluid after exposure to hyperoxia in both IFN-γ−/− mice and wild-type mice, suggesting that hyperoxia initiates upstream events that result in IFN-γ production. Although there was no significant difference in overall survival, IFN-γ−/− mice had a better early survival rate than did the wild-type mice. Therefore, these data strongly suggest that IFN-γ is a key molecular contributor to hyperoxia-induced lung injury.
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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 normoxia until 7 or 14 days of postnatal development (PND). In the carotid body, hyperoxia decreased brain-derived neurotrophic factor (BDNF) protein expression by 93% ( P = 0.04) after a 7-day exposure, followed by a decrease in retrogradely labeled chemoafferents by 55% ( P = 0.004) within the petrosal ganglion at 14 days. Return to normoxia for 1 wk after a 14-day hyperoxic exposure did not reverse this effect. In the nTS, hyperoxia for 7 days: 1) decreased BDNF gene expression by 67% and protein expression by 18%; 2) attenuated upregulation of BDNF mRNA levels in response to acute hypoxia; and 3) upregulated p75 neurotrophic receptor, truncated tropomyosin kinase B (inactive receptor), and cleaved caspase-3. These effects were not observed in the locus coeruleus (LC). Hyperoxia for 14 days also decreased tyrosine hydroxylase levels by 18% ( P = 0.04) in nTS but not in the LC. In conclusion, hyperoxic exposure during early PND reduces neurotrophin levels in the carotid body and the nTS and shifts the balance of neurotrophic support from prosurvival to proapoptotic in the nTS, the primary brain stem site for central integration of sensory and autonomic inputs.
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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.
Full textAbstract:
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 and increased levels of the DNA repair enzyme 8-oxoguanine DNA glycosylase. Bronchoalveolar lavage (BAL) recovered from hyperoxic, inosine-treated rats contained threefold higher levels of active transforming growth factor-β than BAL from rats exposed to hyperoxia alone, and Smad2 was activated in AEC2 isolated from these animals. ERK1/2 was activated both in freshly isolated and 24-h-cultured AEC2 by in vivo inosine treatment, whereas blockade of the MAPK pathway in vitro reduced the protective effect of in the vivo inosine treatment. Together, the data suggest that inosine treatment during hyperoxic exposure results in protective signaling mediated through pathways downstream of MEK. Thus inosine may deserve further evaluation for its potential to reduce hyperoxic damage to the pulmonary alveolar epithelium.
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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.
Full textAbstract:
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 tissues. Immunohistochemical analyses indicate nitrotyrosine staining of alveolar epithelial and interstitial regions. Furthermore, immunoprecipitation followed by Western blot revealed the nitration of surfactant protein A and t1α, proteins specific for alveolar epithelial type II and type I cells, respectively. The increased myeloperoxidase (MPO) activity and total nitrite levels in bronchoalveolar lavage and lung tissue homogenates were observed in hyperoxic lungs. Neutrophils and macrophages isolated from the hyperoxia-exposed rats, when cocultured with a rat lung epithelial L2 cell line, caused a significant protein nitration in L2 cells. Inclusion of nitrite further increased the protein nitration. These studies suggest that protein nitration during hyperoxia may be mediated in part by MPO generated from activated phagocytic cells, and such protein modifications may contribute to hyperoxia-mediated lung injury.
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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 function tests using the whole body plethysmograph and forced oscillation technique, and lung morphometry. There was a significant difference in survival of preterm pups whether they were exposed to normoxia (83.3%) or hyperoxia (55.9%). Hyperoxic exposure was associated with increased tissue damping and elasticity and decreased static compliance compared with normoxic controls ( P < 0.01). Morphometry revealed an increased linear intercept and increased mean wall transection length, which translates to larger alveoli with septal thickening in hyperoxia compared with normoxia ( P < 0.01). In conclusion, the current experimental hyperoxic conditions to which preterm pups are exposed induce the typical clinical features of bronchopulmonary dysplasia. This model will be used to study novel preventive or therapeutic interventions.
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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 polymerase chain reaction. During recovery from hyperoxia, TRX-Tg mice exhibited an improved mean linear intercept length and increased number of secondary septa in lungs compared with the WT mice. Neonatal hyperoxia enhanced the mRNA expression levels of proinflammatory cytokines in the lungs of both TRX-Tg and WT mice. However, interleukin-6, monocyte chemoattractant protein-1, and chemokine (C-X-C motif) ligand 2 mRNA expression levels were reduced in the lungs of TRX-Tg mice compared with the WT mice during recovery from hyperoxia. Furthermore, TRX-Tg mice exhibited reduced macrophage infiltration in lungs during recovery. These results suggest that in newborn mice TRX ameliorates hyperoxic lung injury during recovery likely through the suppression of proinflammatory cytokines.
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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.
Full textAbstract:
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 hyperoxia than in normoxia. Work rate at ventilatory threshold was lower in hypoxia than in normoxia and hyperoxia but above the upper limit of exercise for the submaximal tests. Hypoxia significantly slowed the response of [Formula: see text] both at the onset and end of exercise compared to normoxia and hyperoxia. Hypoxia also modified the response to PRBS exercise, and again there was no difference between normoxia and hyperoxia. These data support the concept that [Formula: see text] kinetics can be slowed from the normoxic response by a hypoxic gas mixture. Key words: [Formula: see text]max, ventilatory threshold, oxygen deficit, pseudorandom binary sequence