Journal of Applied Physiology, Vol 76, Issue 2 516-522, Copyright © 1994 by American Physiological Society
Pulmonary inflammatory cell response to sustained endotoxin administration
C. Z. Wang, D. N. Herndon, L. D. Traber, S. F. Yang, R. A. Cox, H. Nakazawa, R. E. Barrow and D. L. Traber
Shriners Burns Institute, University of Texas Medical Branch, Galveston 77555-1091.
We have developed a model of human sepsis in sheep. Twenty-four hours after
continuous infusion of Escherichia coli endotoxin (lipopolysaccharide) (10
ng.kg-1.min-1) was begun, pulmonary transvascular fluid flux was almost
five times the baseline values, cardiac output was nearly doubled, and mean
arterial pressure was reduced by approximately 20 mmHg. At this time, the
animals were killed and their lungs were fixed by endotracheal installation
of 2.5% glutaraldehyde at 25 cmH2O pressure. Morphometry was performed by
point counting, and data were expressed as relative volume density.
Pulmonary edema and congestion were observed in sheep receiving
lipopolysaccharide, whereas sham controls appeared normal. There was an
increase in interstitial volume density. There was a significant increase
(P < 0.01) in volume density of the pulmonary intravasculature (180%),
interstitial macrophages (270%), and mast cells (240%). The volume
densities of intravascular and interstitial polymorphonuclear neutrophils
also showed a small insignificant increase.
