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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.

Abstract
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.
AuthorsG Zunic, R Pavlović, Z Malicević, V Savić, I Cernak
JournalNitric oxide : biology and chemistry (Nitric Oxide) Vol. 4 Issue 2 Pg. 123-8 (Apr 2000) ISSN: 1089-8603 [Print] United States
PMID10835292 (Publication Type: Journal Article)
CopyrightCopyright 2000 Academic Press.
Chemical References
  • Amino Acids
  • Nitrates
  • Nitrites
  • Nitric Oxide
  • Arginine
Topics
  • Amino Acids (blood)
  • Animals
  • Arginine (metabolism)
  • Blast Injuries (blood, metabolism)
  • Disease Models, Animal
  • Male
  • Nitrates (blood)
  • Nitric Oxide (metabolism)
  • Nitrites (blood)
  • Rabbits
  • Respiratory Distress Syndrome (blood, metabolism)

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