Acetylcholine-induced and nitric oxide-mediated vasodilation in burns

Microvascular endothelial cells actively participate in local regulation of blood flow and blood-tissue exchange by producing various vasoactive subst ances including nitric oxide (NO), This study examined microcirculatory cha nges in the early stage of thermal injury and the NO-related mechanisms. Re sistance arterioles of rat cremaster muscle were observed using intravital microscopy, Arteriolar diameter and how velocity were measured and flow rat e was calculated after administration of various vasoactive agonists in bur ns. In fluid-resuscitated rats with stable systemic blood pressure, microva scular caliber and blood flow were not significantly altered in the first h our following a 25% total body surface area full-thickness scald burn. Topi cal application of acetylcholine (ACh), an endothelium-dependent vasodilato r, increased arteriolar diameter and flow rate in a dose dependent fashion. The dose-responsive effects of ACh were significantly greater in burned ra ts than in sham-burned rats, and the augmentation was blocked by inhibition of NO production with NG-monomethyl-L-arginine (L-NMMA). Topical applicati on of adenosine, an endothelium-independent vasodilator, and sodium nitropr usside, an exogenous NO donor, markedly increased arteriolar diameter and f low rate. The effects were not significantly different in burned and sham-b urned animals, and the adenosine-induced vasodilation was not blocked by L- NMMA. These data suggest that endothelium-dependent and NO-mediated arterio lar dilation is enhanced in the early stage of thermal injury. This effect may play an important role in the pathophysiological events of microcircula tion and blood-tissue exchange in burns. (C) 1998 Academic Press.