ANALYSIS OF REGIONAL HEMODYNAMIC REGULATION IN RESPONSE TO SCALD INJURY

Ultrasonic probes were placed around dog femoral arteries to record bl ood flow. Hind paw scalding with boiling water (5 s) caused a marked i ncrease in ipsilateral femoral blood flow that persisted for the 2-h o bservation period. Contralateral femoral blood flow and systemic and p ulmonary vascular resistances were unchanged. Compared to scald only a nimals, methysergide pretreatment diminished and shortened the femoral vasodilator response to scald (109+/-14 vs 243+/-27 ml/min at 5 min; 59+/-14 vs 191+/-31 ml/min at 2 h). Pretreatment with ritanserin, BW A 1433U83, atropine, ICI 118551, diphenhydramine, ranitidine, meclofenam ate, L-nitro-arginine methyl ester, 3-amino-1,2,4-triazine, and U 3788 3A had no effect on the increased femoral blood flow response to scald , suggesting this vasodilator response is not dependent upon activatio n of seretonergic(2), adenosine(A1), muscarinic, beta(2)-adrenergic, h istaminergic, or histaminergic; receptors, on cyclooxygenase products, endothelium-derived relaxing factor derived from nitric oxide (NO) sy nthase III, NO derived from NO synthase II, or K-ATP channels, respect ively. Methysergide given after burn immediately reduced the augmented femoral blood flow to preburn levels, suggesting the vasodilator resp onse to scald is mediated through continual activation of local seroto nergic(1)-like receptors, which may be target site(s) for therapeutic interventions to influence burn-induced hemodynamic alterations.