Nitric oxide is biosynthesized from the amino acid L-arginine by the enzyme nitric oxide synthase. Nitric oxide is a vasodilator, a neurotransmitter, and may modulate immune function. The experiments presented here were performed to determine whether the synthesis of nitric oxide is increased following experimental burn injury in rats. After a 30% total body surface area burn in 300-g Lewis rats, the urinary output of nitrate, a stable metabolite of nitric oxide, was significantly increased for 8 days postburn compared with that in sham-burned control rats. The origin of the urinary nitrate from L-arginine was demonstrated by administering the stable isotope 15 N 2 -guanido-arginine to burned and sham-burned rats and observing an immediate enrichment of 15 N in nitrate. The amount of administered 15 N recovered as 15 NO 3 was <1% of the administered arginine isotope in both the burned and unburned rats; the recovery of the isotope increased tenfold over baseline recovery in burned rats. The arginine analog N-monomethyl-arginine, an inhibitor of the enzyme nitric oxide synthase, blocked the postburn rise in urinary NO 3 output in burned rats, but did not completely inhibit the output of NO 3 in burn wound-infected rats. Experimental burn injury in rats results in an increase in L-arginine-dependent nitric oxide production and urinary nitrate output.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of Trauma - Injury, Infection and Critical Care|
|State||Published - Jun 1993|
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine