Pulmonary blast injury increases nitric oxide production, disturbs arginine metabolism, and alters the plasma free amino acid pool in rabbits during the early posttraumatic period
G. Zunic et al., Pulmonary blast injury increases nitric oxide production, disturbs arginine metabolism, and alters the plasma free amino acid pool in rabbits during the early posttraumatic period, NITRIC OXID, 4(2), 2000, pp. 123-128
Plasma nitrate + nitrite (nitrates), as final NO products, and free amino a
cid pool (FAAP) characteristics, as indicators of protein/amino acid metabo
lism, were analyzed in the early (30 min) period following blast injury. Th
e experiments were performed on 27 rabbits subjected to pulmonary blast inj
ury (experimental group) or not exposed to overpressure (controls), We repo
rt that pulmonary blast injury (PBI) induces prompt NO overproduction withi
n a very early period. Increased arginine utilization via NO synthase, pres
umably associated with its cleavage by arginase, leads to the depletion of
the arginine level in arterial plasma 30 min following PBI. Impaired balanc
e between arginine utilization and release/resynthesis from endogenous sour
ces causes disturbed nutritional status and urea cycle activity. Early iden
tification and appropriate management of the changes in amino acid metaboli
sm should be included in the evaluation of patients with blast injury. Furt
hermore, the results suggest that depleted arterial levels of arginine and
NO overproduction may be helpful in diagnosis and prognosis of blast injury
. (C) 2000 Academic Press.