2006 OPEN FORUM Abstracts
LIPOPOLYSACCHARIDE (LPS) INFUSION OVER A 5 HOUR PERIOD CAUSES LUNG INJURY IN SWINE
Marcia Volpe RPT, Alexander Adams FAARC, RRT,
John Marini MD, Joel Holger MD.,
Healthpartners/Regions Hospital, St. Paul, Minnesota and Sao Paulo, Brazil.
Background:
Animal models employed to cause and study lung injury includes saline lavage,
oleic acid infusion, and pneumonia induced by direct bacterial instillation. In
studies of ARDS patients, sepsis and/or shock frequently precede and coexist
with the development of ARDS. Animal models of shock include a steady infusion of
the endotoxin lipopolysaccharide (LPS) or cecal ligation with puncture to
create hypo and hyper dynamic shock conditions. In a study of insulin/glucose
treatment for shock we identified and tracked lung injury development during
the administration of LPS.
Methods: After
deep anesthesia and preparation that included arterial access and right heart
catheterization, we infused 20 mgm/kg/hr of LPS for 5 hours to 6 juvenile swine. Ventilation
was adjusted to maintain adequate gas exchange but a standardized assessment
setting of pressure controlled ventilation at 20 cmH2O was applied
every 30 min.
Results: After 30
minutes of LPS infusion, compliance and gas exchange deteriorated rapidly (figure)
followed by a recovery and an eventual continuing decline. Pulmonary artery
pressure markedly increased and cardiac output dropped during the initial phase
of LPS infusion. Post mortem WW/DW ratios exhibited lung edema formation (6.77 ±
0.95) compared to our laboratory standard of 5.5 for normal pig lungs.
Conclusions: LPS infusion caused a
significant reduction in oxygenation and moderate reduction in compliance with
an increase in WW/DW. The cardiovascular effects of LPS infusion were similar
to the pattern seen in oleic acid injury. Sub-lethal infusions of LPS can model
lung injury associated with shock.