Journal of Applied Physiology, Vol 68, Issue 4 1688-1695, Copyright © 1990 by American Physiological Society
Pathogenesis of pulmonary edema associated with intracisternal endotoxin in dogs
A. Nahum, L. D. Wood, G. Crawford, R. Ripper, L. Segil and J. I. Sznajder
Section of Pulmonary and Critical Care Medicine, Michael Reese Hospital and Medical Center, Chicago, Illinois.
To examine the role of central nervous system injury in the pathogenesis of
pulmonary edema, we injected Escherichia coli endotoxin (5 mg/kg) into the
cisterna magna of six dogs (group E) and compared, over 4 h, both the
pulmonary edema and cerebrospinal fluid (CSF) abnormalities with those in
six control dogs (group C). In group E, intracisternal endotoxin raised
intracranial pressure from 21 +/- 6 to 38 +/- 8 cmH2O (P less than 0.001),
CSF total protein from 18 +/- 6 to 54 +/- 19 mg/dl (P less than 0.001), and
CSF malondialdehyde from 0.12 +/- 0.11 to 0.61 +/- 0.35 nmol/ml (P less
than 0.05); all were unchanged in group C. When the pulmonary wedge
pressure was maintained at 10 mmHg by fluid infusion, extravascular thermal
volume in group E increased from 7.2 +/- 1.2 to 12.0 +/- 2.7 ml/kg (P less
than 0.005) at 4 h when the excised lungs weighed 13.6 +/- 1.5 g/kg; in
group C, extravascular thermal volume did not increase, and the excised
lungs weighed less (10.8 +/- 1.3 g/kg, P less than 0.05) than those in
group E. The dry weights of the lungs were not different between groups,
and the alveolar lining fluid-to-plasma albumin ratio in both groups
remained low, 0.1-0.2. Fluid infusion in group E (9.2 +/- 2.9 liters)
caused colloid oncotic pressure to decrease 4.5 +/- 2.8 mmHg; colloid
oncotic pressure fell less (0.8 +/- 1.9 mmHg, P less than 0.001) in group C
as less fluid (2.2 +/- 1.5 liters, P less than 0.001) was required to
maintain pulmonary wedge pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
