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in smoke inhalation lung injury
1 Pulmonary and Critical Care Unit, Department of Medicine, Massachusetts General Hospital, Shriners Burns Institute, and Harvard Medical School, Boston, Massachusetts 02114; and 2 Growth Biology Laboratory, Livestock and Poultry Institute, United States Department of Agriculture, Beltsville, Maryland 20705
Received 9 October 1996; accepted in final form 20 December 1996.
Hales, Charles A., T. H. Elsasser, Peter Ocampo, and Olga
Efimova. TNF-
in smoke inhalation lung injury.
J. Appl. Physiol. 82(5):
1433-1437, 1997.
Adult respiratory distress syndrome is a major
cause of morbidity in fire victims. Tumor necrosis factor-
(TNF-
)
is edematogenic and has been associated with the etiology of other
forms of adult respiratory distress syndrome. In the sheep lymph
fistula model, we measured TNF-
after 48 (n = 7) or 128 (n = 3) breaths of cotton smoke and
compared this with sham controls (n = 5) or controls in which left atrial pressure was elevated to 20 mmHg
(n = 5) to increase lymph flow in the absence of inflammation. Smoke induced a rise in lymph flow and pulmonary arterial pressure with either no fall in lymph-to-plasma protein ratio (128 breaths) or a modest fall in lymph-to-plasma protein
ratio (48 breaths), consistent with a change in microvascular permeability as well as a rise in microvascular pressure.
Lymph concentration of TNF-
fell in both groups, although lymph flux (concentration × flow) transiently rose in both. In neither case did TNF-
flux exceed that induced by left atrial pressure elevation. TNF-
was detectable in only one out of five sheep in alveolar lavage. Thus, by utilizing a sensitive and specific radioimmunoassay, we were unable to demonstrate a role for TNF-
in smoke-induced microvascular lung injury in sheep.
lung lymph; acute lung injury; sheep; tumor necrosis
factor-
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