The purpose of this study is to elucidate the mechanism and pathophysiology of reflex sympathetic dystrophy, a condition of vascular dysautonomia, by 1) studying changes in regional blood flow, pain levels, and catecholamine dynamics, and 2) by measuring regional norepinephrine spillover and neuronal removal of norepinephrine using an infusion of tritiated 1-norepinephrine and tritiated d, 1-isoproterenol, before and after regional sympathetic blockage. Thus, we should be able to determine whether there is an increase in Uptake 1 or norepinephrine in reflex sympathetic dystrophy, whether there is a defect in Uptake 1, or whether increased norepinephrine is present. If RSD is due to excessive alpha 1 activity, there should then be decreased resistance to alpha 1 blockage, of clinical significance in the treatment of this poorly understood syndrome.
