Vascular changes following deep skin burns are characterised by vasoconstriction and progressive ischemia. Nitric oxide (NO) has been shown to be a potent regulator of vascular smooth muscle tone and tissue perfusion. We assessed the importance of NO on post-burn skin perfusion in rats using laser Doppler. The present results show that neither the NO-synthase inhibitor, NG-nitro- l-arginine ( l-NNA) ( n=6) nor the NO precursor, l-arginine, significantly influenced skin perfusion in nonburned skin compared to saline-treated animals. In the area of full-thickness skin burn, neither l-arginine ( n=6) nor l-NNA ( n=6) had significant influence on post-burn perfusion compared to saline-treated controls ( n=6). Administration of l-NNA ( n=6) significantly impaired skin perfusion in the area adjacent to the contact burn representing a partial-thickness burn, while the NO precursor, l-arginine ( n=6) had no significant effect on burn perfusion as compared to saline-treated controls ( n=6). In conclusion, impairment of perfusion in a full thickness burn following administration of NO-synthase inhibitor suggests that nitric oxide is involved in the mechanisms responsible for maintaining adequate circulation post-burn. The lack of additional improvement of perfusion in response to l-arginine may suggest that NO synthesis in response to the thermal trauma is already at a peak.