Journal of Applied Physiology, Vol 61, Issue 4 1395-1402, Copyright © 1986 by American Physiological Society
Endotoxin increases pulmonary vascular protein permeability in the dog
C. H. Welsh, I. M. Dauber and J. V. Weil
Endotoxin increases pulmonary vascular permeability consistently in some
species but fails to reliably cause injury in the dog. We wondered whether
this phenomenon depended on the method of injury assessment, as others have
relied on edema measurement; we quantified injury by monitoring the rate of
extravascular protein accumulation. 113mIn-labeled protein and
99mTc-labeled erythrocytes were injected into anesthetized dogs and
monitored by an externally placed lung probe. A protein leak index, the
rate of extravascular protein accumulation, was derived from the rate of
increase in lung protein counts corrected for changes in intravascular
protein activity. After administration of Salmonella enteriditis endotoxin
(4 micrograms/kg), the protein leak index was elevated 2.5-fold (41.1 +/-
4.6 X 10(-4) min-1) compared with control (16.0 +/- 2.8 X 10(-4) min-1). In
contrast, wet-to-dry weight ratios failed to increase after endotoxin (4.6
+/- 0.8 vs. control values of 4.2 +/- 0.5 g/g dry bloodless lung). However,
we observed that endotoxin increased lung dry weight (per unit body
weight), which may have attenuated the change in wet-to-dry weight ratios.
To determine whether low microvascular pressures following endotoxin
attenuated edema formation, we increased pulmonary arterial wedge pressures
in five dogs by saline infusion, which caused an increase in wet-to-dry
weight ratios following endotoxin but no change in the five controls. We
conclude that low dose endotoxin causes pulmonary vascular protein leak in
the dog while edema formation is minimal or absent.
