Consequences of Hyperoxia and the Toxicity of Oxygen in the Lung
Oxygen (O2) is life essential but as a drug has a maximum positive biological benefit and accompanying toxicity effects. Oxygen is therapeutic for treatment of hypoxemia and hypoxia associated with many pathological processes. Pathophysiological processes are associated with increased levels of hype...
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| Format: | Article |
| Language: | English |
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Wiley
2011-01-01
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| Series: | Nursing Research and Practice |
| Online Access: | http://dx.doi.org/10.1155/2011/260482 |
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| _version_ | 1832549216952516608 |
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| author | William J. Mach Amanda R. Thimmesch J. Thomas Pierce Janet D. Pierce |
| author_facet | William J. Mach Amanda R. Thimmesch J. Thomas Pierce Janet D. Pierce |
| author_sort | William J. Mach |
| collection | DOAJ |
| description | Oxygen (O2) is life essential but as a drug has a maximum positive biological benefit and accompanying toxicity effects. Oxygen is therapeutic for treatment of hypoxemia and hypoxia associated with many pathological processes. Pathophysiological processes are associated with increased levels of hyperoxia-induced reactive O2 species (ROS) which may readily react with surrounding biological tissues, damaging lipids, proteins, and nucleic acids. Protective antioxidant defenses can become overwhelmed with ROS leading to oxidative stress. Activated alveolar capillary endothelium is characterized by increased adhesiveness causing accumulation of cell populations such as neutrophils, which are a source of ROS. Increased levels of ROS cause hyperpermeability, coagulopathy, and collagen deposition as well as other irreversible changes occurring within the alveolar space. In hyperoxia, multiple signaling pathways determine the pulmonary cellular response: apoptosis, necrosis, or repair. Understanding the effects of O2 administration is important to prevent inadvertent alveolar damage caused by hyperoxia in patients requiring supplemental oxygenation. |
| format | Article |
| id | doaj-art-1ab52e058222451a817b29d802358ace |
| institution | Kabale University |
| issn | 2090-1429 2090-1437 |
| language | English |
| publishDate | 2011-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Nursing Research and Practice |
| spelling | doaj-art-1ab52e058222451a817b29d802358ace2025-02-03T06:11:44ZengWileyNursing Research and Practice2090-14292090-14372011-01-01201110.1155/2011/260482260482Consequences of Hyperoxia and the Toxicity of Oxygen in the LungWilliam J. Mach0Amanda R. Thimmesch1J. Thomas Pierce2Janet D. Pierce3School of Nursing, University of Kansas, 3901 Rainbow Boulevard, Kansas City, KS 66160, USASchool of Nursing, University of Kansas, 3901 Rainbow Boulevard, Kansas City, KS 66160, USAU.S. Department of Veterans Affairs (122), Rehabilitation Research and Development Service, 810 Vermont Avenue, NW, Washington, DC 20420, USASchool of Nursing, University of Kansas, 3901 Rainbow Boulevard, Kansas City, KS 66160, USAOxygen (O2) is life essential but as a drug has a maximum positive biological benefit and accompanying toxicity effects. Oxygen is therapeutic for treatment of hypoxemia and hypoxia associated with many pathological processes. Pathophysiological processes are associated with increased levels of hyperoxia-induced reactive O2 species (ROS) which may readily react with surrounding biological tissues, damaging lipids, proteins, and nucleic acids. Protective antioxidant defenses can become overwhelmed with ROS leading to oxidative stress. Activated alveolar capillary endothelium is characterized by increased adhesiveness causing accumulation of cell populations such as neutrophils, which are a source of ROS. Increased levels of ROS cause hyperpermeability, coagulopathy, and collagen deposition as well as other irreversible changes occurring within the alveolar space. In hyperoxia, multiple signaling pathways determine the pulmonary cellular response: apoptosis, necrosis, or repair. Understanding the effects of O2 administration is important to prevent inadvertent alveolar damage caused by hyperoxia in patients requiring supplemental oxygenation.http://dx.doi.org/10.1155/2011/260482 |
| spellingShingle | William J. Mach Amanda R. Thimmesch J. Thomas Pierce Janet D. Pierce Consequences of Hyperoxia and the Toxicity of Oxygen in the Lung Nursing Research and Practice |
| title | Consequences of Hyperoxia and the Toxicity of Oxygen in the Lung |
| title_full | Consequences of Hyperoxia and the Toxicity of Oxygen in the Lung |
| title_fullStr | Consequences of Hyperoxia and the Toxicity of Oxygen in the Lung |
| title_full_unstemmed | Consequences of Hyperoxia and the Toxicity of Oxygen in the Lung |
| title_short | Consequences of Hyperoxia and the Toxicity of Oxygen in the Lung |
| title_sort | consequences of hyperoxia and the toxicity of oxygen in the lung |
| url | http://dx.doi.org/10.1155/2011/260482 |
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