Atrial Electrophysiology in Experimental Hyperthyroidism in Rabbits

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Abstract
Male rabbits received l-thyroxine (250 µg/kg) subcutaneously for 7 days and exhibited marked tachycardia, elevation of protein-bound iodine levels and a 26% mean weight loss. Their hearts were isolated and perfused by the Langendorff technique. In 8 thyroid-treated rabbits the mean heart rate before they were killed and also after 30 minutes of perfusion was much higher than that of 10 controls; threshold in late diastole was lower, and the mean effective refractory period was shorter: 109 msec (95 to 116) as compared with 147 msec (130 to 170). The atrial multiple-response threshold was strikingly lower, and strength-interval curves were shifted to the left without overlap or change in contour. Atropine, 7 µg/liter, did not significantly affect these changes. Acute perfusion of four hearts with l-thyroxine (500 µg/liter) produced similar, but less consistent, results. Perfusion with either epinephrine or norepinephrine, regardless of concentration, could not reproduce the changes seen with thyroid treatment. It is concluded that thyroxine profoundly alters electrophysiologic variables of atrial tissue independently of the autonomic nervous system and that these changes are responsible for many cardiac effects of hyperthyroidism, including the enhanced susceptibility to atrial fibrillation in thyrotoxicosis.

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