Relevant bibliographies by topics / Hyperoxia

Academic literature on the topic 'Hyperoxia'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 March 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Hyperoxia.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Hyperoxia"

1

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 (September 1, 1999): L636—L644. http://dx.doi.org/10.1152/ajplung.1999.277.3.l636.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
2

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 (June 1, 2002): H2414—H2421. http://dx.doi.org/10.1152/ajpheart.00947.2001.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
3

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 (August 2005): L307—L314. http://dx.doi.org/10.1152/ajplung.00030.2005.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
4

Buckley, S., W. Shi, L. Barsky, and 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, no. 4 (April 2008): L739—L748. http://dx.doi.org/10.1152/ajplung.00294.2007.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
5

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 (February 2004): 784–91. http://dx.doi.org/10.1152/japplphysiol.00892.2003.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
6

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 (April 2017): 058–67. http://dx.doi.org/10.4322/jms.113617.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
7

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 (November 2006): L966—L975. http://dx.doi.org/10.1152/ajplung.00045.2006.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
8

Patel, Vivek, Katelyn Dial, Jiaqi Wu, Alex G. Gauthier, Wenjun Wu, Mosi Lin, Michael G. Espey, Douglas D. Thomas, Charles R. Ashby, and Lin L. Mantell. "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 (February 1, 2020): 977. http://dx.doi.org/10.3390/ijms21030977.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
9

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 (July 2006): H210—H215. http://dx.doi.org/10.1152/ajpheart.01168.2005.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
10

Schauer, Steven G., Michael D. April, Jason F. Naylor, Nee-Kofi Mould-Millman, Vikhyat S. Bebarta, Tyson E. Becker, Joseph K. Maddry, and Adit A. Ginde. "Incidence of Hyperoxia in Combat Wounded in Iraq and Afghanistan: A Potential Opportunity for Oxygen Conservation." Military Medicine 184, no. 11-12 (May 29, 2019): 661–67. http://dx.doi.org/10.1093/milmed/usz125.

Full text
Abstract:
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 mmHg and extreme hyperoxia &gt; 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.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Hyperoxia"

1

Tähepõld, Peeter. "Myocardial protection by hyperoxia /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-247-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Cox, April. "Effects of hyperoxia in alzheimers transgenic mice." Scholar Commons, 2005. http://scholarcommons.usf.edu/etd/2836.

Full text
Abstract:
An association between major surgery in the elderly and precipitation of Alzheimers disease (AD) has been reported. Hyperoxia (100%) oxygen is commonly administered after surgery to increase the oxygen content of blood. However, hyperoxia is a potent cerebral vasoconstrictor and generator of free radicals, as is [beta]amyloid (A[beta];). This study was aimed at examining behavioral, neuropathological, and neurochemical effects of hyperoxia treatments in APPsw transgenic mice (Tg+), which have elevated brain A[beta]; levels by 3-4 months of age but are not yet cognitively-impaired. At 3 months of age, Tg+ mice were pre-tested in the radial arm water maze (RAWM) task of working memory and found to be unimpaired. At 4.5 months of age, half of the Tg+ mice received the first of 3 equally-spaced hyperoxia sessions (3 hrs each) given over the ensuing 3 months. The other half of the Tg+ mice were exposed to compressed air during these 3 sessions. RAWM testing performed immediately following the final gas session at 7.5 months of age revealed significant working memory impairment in Tg+ mice exposed to hyperoxia. The Tg+ group that was exposed to placebo treatment showed a trend towards impairment, however, was not significantly different from the non-transgenic group. Hyperoxia-induced memory impairment in Tg+ mice did not involve changes in brain A[beta] deposition, degenerative cell numbers in hippocampus, neocortical lipid peroxidation, or hippocampal levels of APP, ApoE, COX-2, or GFAP. The combination of excess A[beta] and hyperoxia could have induced greater oxidative stress and cerebral vasoconstriction than either one alone, resulting in a pathologic cerebral hypoperfusion that triggered subsequent cognitive impairment.
APA, Harvard, Vancouver, ISO, and other styles
3

Flynn, Erin Patricia. "Experimental infarct mitigation with hyperoxia at normobaric pressure." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0020/MQ55207.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Burghardt, Jacqueline Sarah. "Leukotrienes mediate hyperoxia-induced lung damage in newborn rats." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ34743.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Ruusalepp, Arno. "Signal transduction in restenosis and myocardial protection by hyperoxia /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-705-7/.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Phillips, Gary John. "The role of inflammation in hyperoxia-induced lung injury." Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295865.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Brage, Olivia, and Sara Berglund. "Hyperoxygenering : – I vilken utsträckning exponeras patienter för höga syrgaskoncentrationer under anestesi?" Thesis, Uppsala universitet, Institutionen för folkhälso- och vårdvetenskap, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-325645.

Full text
Abstract:
Det har under en längre tid funnits en stor vilja att under den perioperativa fasen ge patienter höga koncentrationer av syrgas med motiveringen att förbättra vävnadsperfusion och därmed den postoperativa återhämtningen. Nyare studier har påvisat de komplikationer vilka hyperoxygenering skulle kunna medföra i form av ökad mortalitet och morbiditet. Syftet med föreliggande studie var att undersöka huruvida patienter utsätts för hyperoxygenering peroperativt. Studien inkluderade 100 patienter och har genomförts genom en deskriptiv retrospektiv journalgranskning med tillägg av jämförande analyser mellan de undersökta operationsavdelningarna. Huvudresultat för studien var att samtliga undersökta operationsavdelningar hyperoxygenerade patienter under anestesi. För hela det undersökta underlaget uppmättes medelvärdet av parametern maximalt PaO2 till 30,7 ±11,7 kPa och medelvärdet av det genomsnittligt inspiratoriska FiO2 uppmättes till 45,5 ±7,6 %. Det högst uppmätta PaO2-värdet var vid en av de undersökta operationsavdelningarna 66,5 kPa. Slutsatsen vilken kan dras av denna studie är att patienter som undergår anestesi hyperoxygeneras till en nivå som visats innebära ökade risker och hyperoxygenering skulle potentiellt kunna vara ett större peroperativt problem än vad som idag är känt.
For a long period of time, there has been a great desire to provide high concentrations of oxygen in patients during the perioperative phase with the motivation to improve tissue perfusion and postoperative recovery. Recent studies have shown that hyperoxygenation may result in complications such as increased mortality and morbidity. The purpose of the present study was to investigate if patients are exposed to hyperoxygenation perioperatively. The study included 100 patients and was conducted through a descriptive retrospective journal review, with the addition of comparative analyzes between the investigated surgical departments. The main result of the study was that all investigated surgical departments hyperoxygenated patients under anesthesia. For the entire sample material examined, the average parameter of the substrate PaO2 was measured to 30.7 ±11.7 kPa, and the mean of the average inspirational FiO2 was measured to 45,5 ±7,6 %. The highest measured PaO2 value at one of the surgical departments being investigated was 66,5 kPa. In conclusion, the results from this study shows that patients undergoing anesthesia are presently being hyperoxygenated up to a level associated with increased risks, and that hyperoxygenation potentially is a greater peroperative problem than currently known.
APA, Harvard, Vancouver, ISO, and other styles
8

Bustani, Porus C. "The role of hyperoxia in abnormal development of fetal lung." Thesis, University of Leicester, 2007. http://hdl.handle.net/2381/4567.

Full text
Abstract:
Hyperoxia is closely linked with the development of chronic lung disease of prematurity (CLD) but the fixant mechanisms whereby hyperoxia alters lung architecture in the developing lung remain largely unknown.
APA, Harvard, Vancouver, ISO, and other styles
9

Fussell, Julia. "The influence of hyperoxia and dexamethasone on pulmonary protein synthesis." Thesis, University of Southampton, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316304.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Floen, Miranda J. "Thioredoxin-1| Identification of redox substrates and response to hyperoxia." Thesis, University of South Dakota, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10132866.

Full text
Abstract:

Bronchopulmonary dysplasia (BPD) is a serious respiratory complication for the preterm newborn characterized clinically by prolonged respiratory distress and histologically by alveolar simplification and decreased pulmonary vasculature. The development of BPD is well linked to oxidative stress suffered by the newborn as a result of a preterm fetal-neonatal transition, supplemental oxygen, infection, increased inflammation, and mechanical ventilation. Damage suffered by oxidative stress may be through direct mechanisms or through alteration of redox¬sensitive pathways involved in cell death, cell survival, differentiation, and proliferation. Redox¬sensitive modifications regulating protein function and redox-sensitive pathways have mainly been ascribed to oxidative modification of cysteine thiols. As their modification is critical for protein function, maintenance of the thiol redox status is crucial. Thioredoxin-1 (Trx1) functions in maintenance of thiol redox homeostasis, and its redox activity is intimately linked to antioxidant, cytoprotection, proliferation responses, and cytoprotection. While Trx1 targets of redox regulation have been identified, we hypothesize that additional protein may be redox regulated and that Trx1 target profiles may change during oxidative stress. Therefore a novel immunoprecipitation approach, identified as the substrate trap approach, was developed to identify Trx1 targets. The following demonstrates the use of the substrate trap approach for identification of Trx1 redox targets and further application of the approach to identify alterations in target profiles in response to oxidative stress. Use of nuclear targeted substrate trap was successfully employed to enrich from nuclear Trx1 targets. As a final component the characterization of the Trx1 system in mouse from late embryonic development through the first week of life animals were exposed to room air or hyperoxia (model of BPD). Characterization indicates impairment of the Trx1 system in response to hyperoxic injury. As Trx1 is known to regulate proliferation, cell death, survival, differentiation pathways, impairment of the Trx1 system during early neonatal development may potentiate hyperoxic injury and alterations in lung development. Better understanding of Trx1 interactions occur through the substrate trap in a physiological model of BPD will help elucidate redox-signaling pathways involved in BPD pathogenesis.

APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Hyperoxia"

1

A, Sher Neal, ed. Surgery for hyperopia. Thorofare, NJ: Slack Inc., 2004.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Papathanasopoulou, Maira. Ho Ioudas philouse hyperocha: Mythistorēma. Athēna: Ekdoseis Patakē, 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Afanasʹev, Igor B. Superoxide ion: Chemistry and biological implications. Boca Raton: CRC Press, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

1933-, Asada Kozi, and Yoshikawa Toshikazu, eds. Frontiers of reactive oxygen species in biology and medicine: Proceedings of the 6th International Conference on Superoxide and Superoxide Dismutase, Kyoto, Japan, October 11-15, 1993. Amsterdam: Excerpta Medica, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Judd, Sandra J. Eye care sourcebook: Basic consumer health information about vision and disorders affecting the eyes and surrounding structures, including facts about hyperopia, myopia, presbyopia, astigmatism, cataracts, macular degeneration, glaucoma, and other disorders of the cornea, retina, macula, conjunctiva, and optic nerve; along with guidelines for recognizing and treating eye emergencies, advice about protecting the eyes at work, home, and play, tips for living with low vision ... 5th ed. Detroit, MI: Omnigraphics, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Bandali, Karim Sadrudin. The cardiovascular and 'systemic' effects of hyperoxia in the newborn. 2004.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

The relation of maximal oxygen uptake and hyperoxia to reaction and movement times in older men and women. 1985.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

The relation of maximal oxygen uptake and hyperoxia to reaction and movement times in older men and women. 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Beyond saturation: The limits of hyperoxia the effects of high arterial oxygen tensions on myocardial metabolism in the neonate. Ottawa: National Library of Canada, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Tsubota, Kazuo, Dimitri T. Azar, Brian S. Boxer Wachler, and Douglas Koch. Hyperopia and Presbyopia. Taylor & Francis Group, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Hyperoxia"

1

Bulte, Daniel. "Hyperoxia and Functional MRI." In Advances in Experimental Medicine and Biology, 187–99. Boston, MA: Springer US, 2016. http://dx.doi.org/10.1007/978-1-4899-7678-9_13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Roux, P. "Normoxia and Hyperoxia in Neuroprotection." In Annual Update in Intensive Care and Emergency Medicine 2014, 93–104. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-03746-2_8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Thews, O., D. K. Kelleher, and P. Vaupel. "Tumor Oxygenation Under Normobaric and Hyperbaric Hyperoxia." In Advances in Experimental Medicine and Biology, 79–87. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5399-1_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Harijith, Anantha K., and Vineet Bhandari. "Hyperoxia in the Pathogenesis of Bronchopulmonary Dysplasia." In Bronchopulmonary Dysplasia, 3–26. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28486-6_1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Miyamoto, Y., and K. Niizeki. "Ventilatory Responses During Ramp Exercise in Hyperoxia." In Advances in Experimental Medicine and Biology, 147–52. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1933-1_30.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Bitterman, H., V. Brod, and N. Bitterman. "Hemodynamic Effects of Hyperoxia in Hemorrhagic Shock." In Anaesthesia, Pain, Intensive Care and Emergency Medicine - A.P.I.C.E., 453–58. Milano: Springer Milan, 1998. http://dx.doi.org/10.1007/978-88-470-2278-2_48.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Bisgard, Gerald, Julie Wenninger, Zunyi Wang, and E. Burt Olson. "Environmental Hyperoxia and Development of Carotid Chemoafferent Function." In Integration in Respiratory Control, 30–34. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-73693-8_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Ahotupa, M., E. Mantyla, V. Peltola, A. Puntala, and Hannu Toivonen. "Pro Oxidant Effects of Normobaric Hyperoxia in Rat Tissues." In Vascular Endothelium, 290. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3736-6_60.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Sabourin, Patrick J., Kristen J. Nikula, Amie J. Birdwhistell, Breton C. Freitag, and Jack R. Harkema. "Biochemical and Morphologic Response of Nasal Epithelia to Hyperoxia." In Advances in Experimental Medicine and Biology, 813–16. Boston, MA: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4684-5877-0_112.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Messmer, Catalina, Pedro Cabrales, and Marcos Intaglietta. "Effects of Acute Anemia and Hyperoxia on Oxygen Distribution." In Oxygen Transport to Tissue XXXIII, 213–18. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-1566-4_31.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Hyperoxia"

1

Bizios, R., L. A. Holleran, T. P. Ladd, and R. D. Iveson. "EFFECTS OF HYPER0XIC AND HYPOXIC CONDITIONS ON ALBUMIN TRANSPORT ACROSS CULTURED ENDOTHELIAL MONOLAYERS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643361.

Full text
Abstract:
Transport of albumin across cultured bovine pulmonary artery endothelial monolayers was studied under control (ambient air), hyperoxic (95% O2, 5% CO2) and hypoxic (95% N2, 5% CO2) conditions at 37°C over 3 hours. The experimental system consisted of two compartments separated by the endothelial monolayer grown to confluence on a gelatinized polycarbonate membrane (0.8 μm pore diameter). Albumin (4 gm% in PBS) solution and PBS buffer were placed on the luminal and abluminal sides of the confluent endothelial monolayer respectively. Albumin concentrations in the abluminal compartment at various time intervals were determined (Lowry assay) and the results are shown in the table.Compared to control, exposure to hyperoxia resulted in increased albumin transendothelial transport by one order of magnitude for time intervals up to 1 hr, and by over 50% for later times. In contrast albumin transendothelial transport under hypoxic conditions was comparable to the results obtained under control conditions. The results of this study indicate that hyperoxia greatly affects the transport properties of endothelium. (Supported by the Whitaker Foundation.)
APA, Harvard, Vancouver, ISO, and other styles
2

Gauthier, A., R. Sitapara, and L. Mantell. "GAT107 Attenuates Hyperoxia-Induced Macrophage Dysfunction." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2093.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Buczynski, Bradley W., Ysabella Esteban, Min Yee, Joshua L. Allen, Katherine Bachmann, Deborah A. Cory-Slechta, and Michael A. O'Reilly. "Neonatal Hyperoxia Disrupts Neurobehavior In Adult Mice." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1818.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Kolliputi, Narasaiah, Rahamthulla S. Shaik, and Aaron B. waxman. "Extracellular Atp Triggers Hyperoxia-Induced Lung Inflammation." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2105.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Dumpa, Vikramaditya, Lori Nielsen, Huamei Wang, and Vasanth HS Kumar. "Caffeine Modulates Hyperoxia- Induced Angiogenesis in Newborn Mice." In Selection of Abstracts From NCE 2015. American Academy of Pediatrics, 2017. http://dx.doi.org/10.1542/peds.140.1_meetingabstract.82.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Yang, Guang, Chhanda Biswas, Ping La, Amal P. Fernando, Alexandra Selby, and Phyllis A. Dennery. "Heme Oxygenase-1 Modulates Nrf2 Activation In Hyperoxia." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1963.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Yazdani, Sasan, Nicolas Bourdillon, AltitudeOmics Group, and Jean-Marc Vesin. "Effect of Hypoxia and Hyperoxia on Baroreflex Sensitivity." In 2016 Computing in Cardiology Conference. Computing in Cardiology, 2016. http://dx.doi.org/10.22489/cinc.2016.151-347.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Tikhonov, Michail A., Victor M. Baranov, and Alexander N. Kotov. "Immersion, Hyperoxia, Hypercapnia: Additive Effect Upon Pulmonary Function." In International Conference On Environmental Systems. 400 Commonwealth Drive, Warrendale, PA, United States: SAE International, 1994. http://dx.doi.org/10.4271/941261.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

You, K., P. Parikh, K. Khandalavala, S. A. Wicher, B. Yang, A. M. Roesler, L. Manlove, B. Roos, C. M. Pabelick, and Y. S. Prakash. "Moderate Hyperoxia Induces Senescence in Human Fetal Lung Fibroblasts." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5494.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Lozon, TI, and WA Altemeier. "CHOP Deficient Mice Have Augmented Lung Injury with Hyperoxia." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4168.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Hyperoxia"

1

Mehm, William J. Effect of Barbiturates and Hyperoxia on Lipid Peroxidation in Hypoxic Neurons. Fort Belvoir, VA: Defense Technical Information Center, April 1993. http://dx.doi.org/10.21236/ada278467.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Shykoff, B. Incidence of CNS Oxygen Toxicity with Mild Hyperoxia: A Literature and Data Review. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada607392.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Dougherty, J. H., Eckenhoff Jr., Hunter R. G., Jr W. L., J. W. Parker, and D. J. Styer. Hyperbaric and Hyperoxic Effects on Pulmonary Function During Air Saturation Dives. Fort Belvoir, VA: Defense Technical Information Center, July 1985. http://dx.doi.org/10.21236/ada418606.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Zupan, Michael F., Dustin R. Bakkie, Jennifer A. Malagon, Jessica A. Malagon, and Kristin Perdue. Comparison of the 1.5 Mile Run Times at 7,200 Feet and Simulated 850 Feet in a Hyperoxic Room. Fort Belvoir, VA: Defense Technical Information Center, March 2012. http://dx.doi.org/10.21236/ada567837.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Zupan, Michael F., Dustin R. Bakkie, Jennifer A. Malagon, Jessica A. Malagon, and Kristin Perdue. Comparison of the 1.5 Mile Run Times at 7,200 Feet and Simulated 850 Feet in a Hyperoxic Room. Fort Belvoir, VA: Defense Technical Information Center, March 2012. http://dx.doi.org/10.21236/ada580886.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Hyperoxia' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography