Plasma
nitrate +
nitrite (
nitrates), as final NO products, and free
amino acid pool (FAAP) characteristics, as indicators of
protein/
amino acid metabolism, were analyzed in the early (30 min) period following
blast injury. The experiments were performed on 27 rabbits subjected to pulmonary
blast injury (experimental group) or not exposed to overpressure (controls). We report that pulmonary
blast injury (PBI) induces prompt NO overproduction within a very early period. Increased
arginine utilization via
NO synthase, presumably associated with its cleavage by
arginase, leads to the depletion of the
arginine level in arterial plasma 30 min following PBI. Impaired balance between
arginine utilization and release/resynthesis from endogenous sources causes disturbed nutritional status and
urea cycle activity. Early identification and appropriate management of the changes in
amino acid metabolism should be included in the evaluation of patients with
blast injury. Furthermore, the results suggest that depleted arterial levels of
arginine and NO overproduction may be helpful in diagnosis and prognosis of
blast injury.