[Skip to Content]
[Skip to Content Landing]
December 21, 1964


JAMA. 1964;190(12):1066-1067. doi:10.1001/jama.1964.03070250048017

Does the sympathetic nervous system participate significantly in the hemodynamic changes of hyperthyroidism? The rapid heart rate and increased cardiac output of thyrotoxic patients have suggested to clinicians that the sympathetic nervous system is an important mediator of the effects of excess thyroid hormone. It has been shown experimentally, moreover, that altering sympathetic impulses by means of epidural block can reverse the metabolic and hemodynamic changes induced by thyroid feeding.1 The study of the relationships of thyroid hormone and the cardiovascular system has been hampered by the fact that conventional adrenergic-blocking drugs such as phentolamine and guanethidine do not effectively prevent beta-adrenergic stimulation of the myocardium. The availability of the new compound, pronethalol, which appears to be a specific adrenergic beta-receptor antagonist, provided the opportunity for Wilson and associates2 to study the pharmacodynamic effects of beta-adrenergic receptor blockade in patients with hyperthyroidism. These investigators demonstrated that intravenous administration of

First Page Preview View Large
First page PDF preview
First page PDF preview