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Autonomic activation links CNS oxygen toxicity to acute cardiogenic pulmonary injury.

Publication ,  Journal Article
Demchenko, IT; Zhilyaev, SY; Moskvin, AN; Piantadosi, CA; Allen, BW
Published in: Am J Physiol Lung Cell Mol Physiol
January 2011

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.

Duke Scholars

Published In

Am J Physiol Lung Cell Mol Physiol

DOI

EISSN

1522-1504

Publication Date

January 2011

Volume

300

Issue

1

Start / End Page

L102 / L111

Location

United States

Related Subject Headings

  • Sympathetic Nervous System
  • Respiratory System
  • Rats
  • Pulmonary Circulation
  • Oxygen
  • Lung Injury
  • Lung
  • Hyperbaric Oxygenation
  • Hemodynamics
  • Heart Arrest
 

Citation

APA
Chicago
ICMJE
MLA
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Demchenko, I. T., Zhilyaev, S. Y., Moskvin, A. N., Piantadosi, C. A., & Allen, B. W. (2011). Autonomic activation links CNS oxygen toxicity to acute cardiogenic pulmonary injury. Am J Physiol Lung Cell Mol Physiol, 300(1), L102–L111. https://doi.org/10.1152/ajplung.00178.2010
Demchenko, Ivan T., S Yu Zhilyaev, A. N. Moskvin, Claude A. Piantadosi, and Barry W. Allen. “Autonomic activation links CNS oxygen toxicity to acute cardiogenic pulmonary injury.Am J Physiol Lung Cell Mol Physiol 300, no. 1 (January 2011): L102–11. https://doi.org/10.1152/ajplung.00178.2010.
Demchenko IT, Zhilyaev SY, Moskvin AN, Piantadosi CA, Allen BW. Autonomic activation links CNS oxygen toxicity to acute cardiogenic pulmonary injury. Am J Physiol Lung Cell Mol Physiol. 2011 Jan;300(1):L102–11.
Demchenko, Ivan T., et al. “Autonomic activation links CNS oxygen toxicity to acute cardiogenic pulmonary injury.Am J Physiol Lung Cell Mol Physiol, vol. 300, no. 1, Jan. 2011, pp. L102–11. Pubmed, doi:10.1152/ajplung.00178.2010.
Demchenko IT, Zhilyaev SY, Moskvin AN, Piantadosi CA, Allen BW. Autonomic activation links CNS oxygen toxicity to acute cardiogenic pulmonary injury. Am J Physiol Lung Cell Mol Physiol. 2011 Jan;300(1):L102–L111.

Published In

Am J Physiol Lung Cell Mol Physiol

DOI

EISSN

1522-1504

Publication Date

January 2011

Volume

300

Issue

1

Start / End Page

L102 / L111

Location

United States

Related Subject Headings

  • Sympathetic Nervous System
  • Respiratory System
  • Rats
  • Pulmonary Circulation
  • Oxygen
  • Lung Injury
  • Lung
  • Hyperbaric Oxygenation
  • Hemodynamics
  • Heart Arrest