Pathogenesis of pulmonary edema associated with intracisternal endotoxin in dogs

A. Nahum*, L. D H Wood, G. Crawford, R. Ripper, L. Segil, J. I. Sznajder

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

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 < 0.001), CSF total protein from 18 ± 6 to 54 ± 19 mg/dl (P < 0.001), and CSF malondialdehyde from 0.12 ± 0.11 to 0.61 ± 0.35 nmol/ml (P < 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 < 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 < 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 < 0.001) in group C as less fluid (2.2 ± 1.5 liters, P < 0.001) was required to maintain pulmonary wedge pressure. Venous admixture increased only in group E from 11 ± 4 to 44 ± 10% (P < 0.001); venous admixture at 4 h was large for the small increase in lung edema and correlated with CSF malondialdehyde (r = 0.85, P < 0.01). We conclude that intracisternal endotoxin caused central nervous system injury and required massive fluid infusion, which caused dilutional pulmonary edema without an increase in pulmonary vascular pressures. Conceivably, the intrapulmonary shunt was exaggerated by the brain injury and/or the increased pulmonary blood flow associated with the high cardiac output resembling human septic shock and canine intravenous endotoxin shock.

Original languageEnglish (US)
Pages (from-to)1688-1695
Number of pages8
JournalJournal of applied physiology
Volume68
Issue number4
DOIs
StatePublished - 1990

Keywords

  • lipid peroxidation
  • meningitis

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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