Why the study?
Does local infusion of noradrenaline reveal increased venous alpha-adrenoceptor responsiveness in patients with reflex sympathetic dystrophy compared to normal controls?
Does local infusion of noradrenaline reveal increased venous alpha-adrenoceptor responsiveness in patients with reflex sympathetic dystrophy compared to normal controls?
Patients with reflex sympathetic dystrophy exhibit marked vascular alpha-adrenoceptor hyper-responsiveness to noradrenaline, providing direct evidence for this mechanism in humans.
Supports alpha-adrenoceptor hyper-responsiveness in reflex sympathetic dystrophy; leaves open therapeutic implications pending prospective studies.
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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J. Malcolm O. Arnold (1993) studied this question.
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