The interrelationships of thyroid hormone, the adrenal medulla, and the sympathetic nervous system have been recognized since the early part of the present century (1-4). More recent studies of experimental hyperthyroidism by Brewster, Isaacs, Osgood, and King (5) supported the hypothesis that the sympathetic nervous system may be responsible for the metabolic and hemodynamic changes associated with the hypermetabolic state, since the alterations induced by thyroid feeding could be reversed by epidural block.Recent trials of reserpine (6, 7) and guanethidine (7-9) that release catecholamines and deplete the tissues of them have shown that these drugs can partially alleviate some clinical manifestations of thyrotoxicosis. 'The cardiac rate may be slowed, but consistent and significant reductions of the high cardiac output in patients with hyperthyroidism have not been reported, except by Goldstein, Furth, Becker, and Killip (10) using guanethidine. Methyldopa, a decarboxylase inhibitor, also slows the pulse rate of patients with hyperthyroidism, but does not significantly change the clinical manifestations (11), or reduce the elevated cardiac output or oxygen consumption (12). Furthermore, a continuous infusion of phentolamine (Regitine) in a hyperthyroid patient does not alter cardiac output (13), since it blocks alpha-rather than beta-adrenergic receptors. If the sympathetic nervous system is a crucial mediator of the hemodynamic changes in hyperthyroidism, it seems logical to explore the part that beta

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These experiments were designed to determine if the location of ectopic ventricular stimulation influences ventricular performance. Heart block was produced in dogs by ligating the A-V bundle. Small bipolar electrodes were implanted in the apex, high lateral wall, and posterior septal region in six dogs. Several days after recovery dye dilution cardiac outputs, femoral arterial, and right atrial pressures were measured while stimulating from each of the three sites at varying rates between 60 and 240 beats/min. Mean cardiac outputs from stimulation at each of the three sites were similar and their 95% confidence intervals overlapped. Mean systemic pressure did not change significantly with frequency or location of ventricular stimulation. The experiments suggest that the pathway of ventricular activation does not affect ventricular function in complete heart block.

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