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.