Citation

Kramer GC, Herndon DN, Linares HA, Traber DL. J. Burn Care Rehabil. 1989; 10(1): 45-51.

Affiliation

Firefighters Pacific Burns Institute, University of California, Davis.

Copyright

(Copyright © 1989, Lippincott Williams and Wilkins)

DOI

unavailable

PMID

2921258

Abstract

We measured airway blood flow in unanesthetized sheep under control conditions and after lung injury induced by inhalation of cotton smoke. Blood flows in trachea, carina, main stem bronchi, intraparenchymal bronchi, and whole lung were measured by injection of radioactive microspheres. In 10 control sheep mean blood flow (+/- SD) was trachea, 17.2 +/- 10.5; main stem bronchi, 17.5 +/- 7.6; and whole lung (parenchyma inclusive of all small intraparenchymal airways), 20.5 +/- 11.9 ml.min-1/100 gm tissue weight. After injury, measurements were made 8 to 30 hours after smoke inhalation when respiratory distress was evident by arterial oxygen tensions of less than 60 mm Hg. Inhalation injury had little effect on cardiac output or blood flow to peripheral tissue. However, after inhalation injury airway blood flow (n = 6) was increased nine times in trachea, eight times in main stem bronchi, twelve times in intraparenchymal bronchi, and two times in whole lung. The increased airway blood flow resulted from a selective vasodilation of the airway vasculature because arterial driving pressures were unchanged by inhalation injury. Other investigators have shown that the microvascular permeability of the bronchial circulation is remarkably sensitive to inflammation, and the present experiments suggest that a selective vasodilation of the airway vasculature is another aspect of the airway response to inflammation. Increased airway blood flow through a leaky microvasculature may increase capillary filtrate from the bronchial circulation and contribute to the pulmonary edema of inhalation injury.

Language: en