Smoke inhalation causes a delayed increase in airway blood flow to primarily uninjured lung areas.
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.


METHODS
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.
Loick
H M
HM
Department of Anesthesiology, University of Texas Medical Branch and Shriners Burns Institute, Galveston, Texas 77550-2788, USA.
Traber
L D
LD
Stothert
J C
JC
Herndon
D N
DN
Traber
D L
DL
D000704:Analysis of Variance; D000818:Animals; D001980:Bronchi / Q000098:blood supply* / Q000293:injuries; D004195:Disease Models, Animal; D005260:Female; D006439:Hemodynamics; D008168:Lung / Q000098:blood supply*; D055370:Lung Injury; D008863:Microspheres; D012123:Pulmonary Ventilation; D012756:Sheep; D015208:Smoke Inhalation Injury / Q000503:physiopathology*; D013152:Splanchnic Circulation; D013997:Time Factors; D014132:Trachea / Q000293:injuries* / Q000503:physiopathology