Citation

Loick HM, Traber LD, Stothert JC, Herndon DN, Traber DL. Intensive Care Med. 1995; 21(4): 326-333.

Affiliation

Department of Anesthesiology, University of Texas Medical Branch and Shriners Burns Institute, Galveston, Texas 77550-2788, USA.

Copyright

(Copyright © 1995, Holtzbrinck Springer Nature Publishing Group)

DOI

unavailable

PMID

7650255

Abstract

OBJECTIVE: Single lung inhalation injury causes tissue damage to the contralateral lung. We therefore examined airway blood flow after smoke inhalation in chronic instrumented sheep to get further information about the underlying pathophysiology. DESIGN/PATIENTS: The right lung and lower trachea of 5 animals were smoke-exposed, while their left lung was air-insufflated using a split ventilation technique. Three animals, where both lungs were only air-insufflated, served as controls. Blood flow to the airway was measured using a labeled microsphere technique. All animals were studied for 24 h following smoke inhalation. Then they were sacrificed and their tissues harvested. RESULTS: The airway blood flow to the smoke-exposed lung was elevated 11-fold immediately after inhalation injury. The bronchial blood flow to the air insufflated lung became significantly elevated 24 h post-smoke, although to a lesser extent. The control animals did not show any changes of bronchial blood flow during the observation time. CONCLUSIONS: Damage to one lung can lead to pathophysiologic changes in the contralateral lung. This response appears to be mediated by hematogenous factors.

Language: en