| Autonomic activation links CNS oxygen toxicity to acute cardiogenic pulmonary injury. | |
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MedLine Citation:
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PMID: 20971806 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Breathing hyperbaric oxygen (HBO₂), particularly at pressures above 3 atmospheres absolute, can cause acute pulmonary injury that is more severe if signs of central nervous system toxicity occur. This is consistent with the activation of an autonomic link between the brain and the lung, leading to acute pulmonary oxygen toxicity. This pulmonary damage is characterized by leakage of fluid, protein, and red blood cells into the alveoli, compatible with hydrostatic injury due to pulmonary hypertension, left atrial hypertension, or both. Until now, however, central hemodynamic parameters and autonomic activity have not been studied concurrently in HBO₂, so any hypothetical connections between the two have remained untested. Therefore, we performed experiments using rats in which cerebral blood flow, electroencephalographic activity, cardiopulmonary hemodynamics, and autonomic traffic were measured in HBO₂ at 5 and 6 atmospheres absolute. In some animals, autonomic pathways were disrupted pharmacologically or surgically. Our findings indicate that pulmonary damage in HBO₂ is caused by an abrupt and significant increase in pulmonary vascular pressure, sufficient to produce barotrauma in capillaries. Specifically, extreme HBO₂ exposures produce massive sympathetic outflow from the central nervous system that depresses left ventricular function, resulting in acute left atrial and pulmonary hypertension. We attribute these effects on the heart and on the pulmonary vasculature to HBO₂-mediated central sympathetic excitation and catecholamine release that disturbs the normal equilibrium between excitatory and inhibitory activity in the autonomic nervous system. |
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Authors:
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Ivan T Demchenko; S Yu Zhilyaev; A N Moskvin; Claude A Piantadosi; Barry W Allen |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. Date: 2010-10-22 |
Journal Detail:
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Title: American journal of physiology. Lung cellular and molecular physiology Volume: 300 ISSN: 1522-1504 ISO Abbreviation: Am. J. Physiol. Lung Cell Mol. Physiol. Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2010-12-20 Completed Date: 2011-01-28 Revised Date: 2012-01-02 |
Medline Journal Info:
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Nlm Unique ID: 100901229 Medline TA: Am J Physiol Lung Cell Mol Physiol Country: United States |
Other Details:
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Languages: eng Pagination: L102-11 Citation Subset: IM |
Affiliation:
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Center for Hyperbaric Medicine and Environmental Physiology, Duke Univ. Medical Center, Durham, NC 27710, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cerebrovascular Circulation / drug effects* Electroencephalography / drug effects Heart / drug effects Heart Arrest / chemically induced Hemodynamics / drug effects Hyperbaric Oxygenation / adverse effects*, methods Lung / drug effects Lung Injury / chemically induced* Oxygen / toxicity* Pulmonary Circulation / drug effects Rats Sympathetic Nervous System / drug effects |
| Grant Support | |
ID/Acronym/Agency:
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R01-AI064789/AI/NIAID NIH HHS |
| Chemical | |
Reg. No./Substance:
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7782-44-7/Oxygen |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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