BACKGROUND: To determine the role of nitric oxide (NO) which is vasodilator agent and inflammatory cytokine, in burn injury. METHODS: Rats were divided into 5 groups, and a 30 % burn was inflicted. In addition to sham control and burn control groups, other 3 groups were given L-Arginine, and L-nitro-L-Arginine methylester (L-NAME), and both. Neutrophil and hematocrit percentage in blood, NO, TNF-alpha and malondialdehyde (MDA) levels in plasma and neutrophil infiltration in the lung were evaluated at 24 hours after thermal injury. RESULTS: The inhibition of NO production with L-NAME treatment significantly decreased these parameters when compared to burned control group. MDA was decreased significantly in all groups which were given drugs. CONCLUSION: The induction and inhibition of NO production both reduced lipid peroxidation but induction increased the mortality, plasma TNF-alpha and neutrophil in the blood. Inhibition of NO production is found more useful after thermal injury in rats.
BACKGROUND: To determine the role of nitric oxide (NO) which is vasodilator agent and inflammatory cytokine, in burn injury. METHODS:Rats were divided into 5 groups, and a 30 % burn was inflicted. In addition to sham control and burn control groups, other 3 groups were given L-Arginine, and L-nitro-L-Arginine methylester (L-NAME), and both. Neutrophil and hematocrit percentage in blood, NO, TNF-alpha and malondialdehyde (MDA) levels in plasma and neutrophil infiltration in the lung were evaluated at 24 hours after thermal injury. RESULTS: The inhibition of NO production with L-NAME treatment significantly decreased these parameters when compared to burned control group. MDA was decreased significantly in all groups which were given drugs. CONCLUSION: The induction and inhibition of NO production both reduced lipid peroxidation but induction increased the mortality, plasma TNF-alpha and neutrophil in the blood. Inhibition of NO production is found more useful after thermal injury in rats.