Vascular changes following deep skin burns are characterised by vasoconstri
ction and progressive ischemia, Nitric oxide (NO) has been shown to be a po
tent regulator of vascular smooth muscle tone and tissue perfusion. We asse
ssed the importance of NO on post-burn skin perfusion in rats using laser D
oppler. The present results show that neither the NO-synthase inhibitor, NG
-nitro-L-arginine (L-NNA) (n = 6) nor the NO precursor, L-arginine, signifi
cantly influenced skin perfusion in nonburned skin compared to saline-treat
ed animals. In the area of full-thickness skin burn, neither L-arginine (Iz
= 6) nor L-NNA (n = 6) had significant influence on post-burn perfusion co
mpared to saline-treated controls (n = 6). Administration of L-NNA (n = 6)
significantly impaired skin perfusion in the area adjacent to the contact b
urn representing a partial-thickness burn, while the NO precursor, L-argini
ne (n = 6) had no significant effect on burn perfusion as compared to salin
e-treated controls (n = 6). In conclusion, impairment of perfusion in a ful
l thickness burn following administration of NO-synthase inhibitor suggests
that nitric oxide is involved in the mechanisms responsible for maintainin
g adequate circulation post-burn. The lack of additional improvement of per
fusion in response to L-arginine may suggest that NO synthesis in response
to the thermal trauma is already at a peak. (C) 2000 Elsevier Science Ltd a
nd ISBI. All rights reserved.