Thyroid Hypocalcemic Principle and Recurrent Laryngeal Nerve Injury as Factors Affecting the Response to Parathyroidectomy in Rats1

Abstract

The extent and time course of the hypocalcemia developing in calcium-depleted young male rats during the first 5 hr after parathyroidectomy were found to differ considerably, depending on which one of 3 methods of parathyroidectomy was used. One hr after the operation the serum calcium of thyroparathyroidectomized rats was higher than that of rats parathyroidectomized alone, whether by excision or hot-wire cautery. By the fifth hr, the serum calcium of rats parathyroidectomized by cautery had fallen much lower, that of rats parathyroidectomized by excision had changed very little, and that of thyroparathyroidectomized rats had decreased, but only to the level of the rats parathyroidectomized by excision. It was found that cutting, stretching or burning the recurrent laryngeal nerves resulted in respiratory difficulty and retarded the fall in serum calcium after parathyroidectomy—results similar to those produced by thyroparathyroidectomy. It was concluded that trauma to these nerves, which is unavoidable during thyroparathyroidectomy, was responsible for the observed retardation in the development of hypocalcemia. The serum calcium of rats parathyroidectomized by excision was further depressed by cautery of the thyroid gland, the effect being greater after bilateral than after unilateral cautery, and by injection of a small amount of rat thyroid extract. It was concluded that the excessive fall in serum calcium of rats parathyroidectomized by cautery was due to the release of a hypocalcemic substance from the thyroid gland. The substance was tentatively named “thyrocalcitonin,” and its relation to “calcitonin,” proposed as a parathyroid hypocalcemic hormone by Copp et al., is discussed.