Importance of nitric oxide in the regulation of burn oedema, proteinuria and urine output

Burn injuries trigger a pronounced inflammatory response in the burned skin, resulting in oedema formation and impaired circulation. This response involves activation of the nitric oxide (NO) synthetic pathway, which could play a key role in the complex hemodynamic and hemostatic changes occurring as a result of a burn trauma. The results presented in full-thickness skin burns of rats show that the NO-precursor, -arginine (n=10), inhibit burn-induced plasma extravasation as compared to saline-treated burned controls (n=10) (p<0.001) to a level not significantly different from nonburned animals. Administration of the NO-synthase inhibitor, NG-nitro- -arginine ( -NNA) (n=10), did not significantly influence burn extravasation compared to burned controls. Accumulated urine volume 90 min post-burn increased ten-fold in burned animals treated with -arginine compared to saline-treated burned controls (p<0.001) and nonburned animals (p<0.001), while -NNA had no significant effect on diuresis. A significantly increased proteinuria occurred in -arginine treated burned animals as compared to burned controls and nonburned controls (p<0.001), whereas -NNA did not significantly influence the leakage of protein in the urine. Activation of NO synthesis significantly suppresses burn edema and strongly increases diuresis along with increased proteinuria.