AIM: To investigate the variation of nitric oxide(NO) and NO synthase(NOS) in rats during the early stage of severe burn and their possible relation with prognosis of severe burns.METHODS: Levels of NO - 2/NO - 3, the metabolic products of NO, nNOS and iNOS protein in brain, lung and duodenum of rats were measured before and after burns. Survival times of rats in each group were also measured.RESULTS: Levels of NO - 2/NO - 3 in rats after burn increased remarkably, selective inducible NOS( iNOS) inhibitor aminoguanidine (AG), and nonselective NOS inhibitor L-NAME can inhibit this increasing. Levels of neuronal NOS(nNOS) protein in normal rats were low, and iNOS could not be detected. Levels of nNOS protein increased mildly in all observed tissues and the levels of iNOS protein increased remarkably after burn. Administration of L-NAME and AG made the increase of nNOS more apparently but could not affect the level of iNOS. Survival time of rats decreased in L-NAME group and increased in AG group compared to control group.CONCLUSION: Symptoms such as vascular ralaxation and hypotension in burn shock are connected mainly with over-increased iNOS. [

AIM: To identify the effects of nitric oxide synthase (NOS) inhibitor on NO production, expression of NOS and mean artery pressure (MAP) in rats with severe burns. METHODS: After administration of non-selective NOS inhibitor, L-NAME, and selective inducible NOS (iNOS) inhibitor, aminoguanidine (AG), to rats with severe burns, levels of NO - 2/NO - 3 in blood, mRNA expression of nerve NOS (nNOS) in lung and duodenum, MAP in each group were calculated. RESULTS: Levels of NO - 2/NO - 3 in blood of rats increased significantly post burn, which could be inhibited by L-NAME and AG, especially by L-NAME. Expression of nNOS mRNA in lung and duodenum of rats increased post burn, which could be enhanced by AG and L-NAME. MAP of rats decreased gradually post burn and administration of AG could slow down this process significantly. CONCLUSION: cNOS and iNOS could play different roles in the pathophysiology of burn shock. Over-expression of iNOS could be closely related to the pathogenesis of burn shock.