Acetylcholine-Induced and Nitric Oxide-Mediated Vasodilation in Burns

摘要: Microvascular endothelial cells actively participate in local regulation of blood flow and blood-tissue exchange by producing various vasoactive substances including nitric oxide (NO). This study examined microcirculatory changes the early stage thermal injury NO-related mechanisms. Resistance arterioles rat cremaster muscle were observed using intravital microscopy. Arteriolar diameter velocity measured rate was calculated after administration agonists burns. In fluid-resuscitated rats with stable systemic pressure, microvascular caliber not significantly altered first hour following a 25% total body surface area full-thickness scald burn. Topical application acetylcholine (ACh), an endothelium-dependent vasodilator, increased arteriolar dose-dependent fashion. The dose-responsive effects ACh greater burned than sham-burned rats, augmentation blocked inhibition NO production NG-monomethyl-l-arginine (L-NMMA). adenosine, endothelium-independent sodium nitroprusside, exogenous donor, markedly rate. different animals, adenosine-induced vasodilation L-NMMA. These data suggest that NO-mediated dilation is enhanced injury. effect may play important role pathophysiological events microcirculation