Abstract
Acute lung injury (ALI) occurs in 44% of patients after hemorrhagic shock (HS) and carries a high morbidity. Polymorphonuclear neutrophils (PMNs) are central to the pathogenesis of post-traumatic ALI. PMNs become primed, with an enhanced response to stimuli after injury and subsequently can induce ALI after a second insult. Succinate is a metabolite that accumulates after injury (up to 700uM from physiologic of 1uM) and has pro-inflammatory effects. We hypothesize that succinate is a causative factor in ALI through PMN priming.
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