Increased Venous Alpha-Adrenoceptor Responsiveness in Patients with Reflex Sympathetic Dystrophy

  1. J. Malcolm O. Arnold, MD;
  2. Robert W. Teasell, MD;
  3. Arthur P. MacLeod, MD;
  4. James E. Brown, MD; and
  5. S. George Carruthers, MD
  1. Requests for Reprints: J. Malcolm O. Arnold, MD, Victoria Hospital, 375 South Street, London, Ontario N6A 4G5, Canada. Acknowledgment: The authors thank Gord Marchiori, PhD, and Amy Lui for assistance in data analysis. Grant Support: Dr. Arnold was supported by a Career Health Scientist Award of the Pharmaceutical Manufacturers Association of Canada.

    Abstract

    Reflex sympathetic dystrophy is a symptom complex characterized by vasomotor instability, hyperesthesia, and pain. Hypothesizing that these symptoms could reflect diminished sympathetic innervation with resultant -adrenoceptor hyper-responsiveness, we studied 11 patients who developed upper-limb reflex sympathetic dystrophy after hemiplegia or trauma and 11 normal controls who were similar in age to the study patients. The diameter of superficial hand veins was measured using a linear variable differential transformer during local infusion of saline and increasing concentrations of noradrenaline. The limbs affected with reflex sympathetic dystrophy showed marked -adrenoceptor hyper-responsiveness; that is, less noradrenaline was required to cause 50% venoconstriction (1.5 compared with 6.8 ng/min, P = 0.001). The unaffected limb in patients with reflex sympathetic dystrophy also showed hyper-responsiveness to noradrenaline when compared with values in normal controls (6.8 compared with 27.4 ng/min, P = 0.01), with such hyper-responsiveness being more marked in patients with hemiplegia. The findings provide the first direct evidence in humans of hyper-responsiveness of vascular -adrenoceptors to noradrenaline in reflex sympathetic dystrophy.

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