Introduction
Overproduction of nitric oxide (NO) is correlated with adverse outcomes in sepsis. NO is additionally a central part of the innate immune system defense against pathogens causing ventilator-associated pneumonia (VAP), which can complicate the clinical course during mechanical ventilation (MV). We hypothesized that pre-exposure to MV and systemic inflammation from endotoxin each would influence bacterial growth in lung tissue, based on an altered immune response in experimental pneumonia. We used a porcine Pseudomonas aeruginosa VAP model with ventilatory and inflammatory pre-exposures before inoculation to evaluate bacterial growth, development of lung damage, total NO production and inflammatory cytokine response.