Catecholamine Depletion in Thyrotoxicosis

AN INTIMATE relationship between the sympathetic nervous system and the cardiovascular effects of thyroid hormone has been extensively documented during the past several decades.'-9 In hyperthyroidism in both man and the experimental animal there is an increased susceptibility to cardiac arrhythmia after parenteral administration of epinephrine.2 4, 0 The frequent occurrence of atrial fibrillation in patients with thyrotoxicosis in the apparent absence of organic heart disease is well known. In addition, hyperthyroidism enhances the pressor effect of injected epinephrine and norepinephrine.7 8 The similarities between the cardiovascular effects of excess thyroid hormone and epinephrine administration have stimulated an evaluation of the therapeutic effects of sympathetic blockade in hyperthyroidism. Spinal anesthesia has been reported to prevent hyperkinetic cardiovascular responses during thyroid surgery.'0 Brewster et al.9 showed that injection of procaine into the epidural space in hyperthyroid dogs reduced the elevated oxygen consumption, heart rate, cardiac output, and blood pressure to control levels. In the treated animals, infusion of epinephrine and norepinephrine restored the hyperthyroid state. They assumed that the procaine had blocked spinal autonomic outflow and concluded that there is an augmentation of the physiologic actions of epinephrine and norepinephrine in thyrotoxicosis.