| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Biological Research Laboratories, Harvard School of Dental Medicine, and Department of Pharmacology, Harvard Medical School Boston, Massachusetts
This investigation was supported in part by a research grant (A-1787) from the National Institute for Arthritis and Metabolic Diseases, USPHS.
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.
Footnotes
1 Presented in part at the 47th Annual Meeting of the Federation of American Societies for Experimental Biology, Atlantic City, New Jersey, April 16-20, 1963 (Fed. Proc. 22: 676, 1963).
2 Present address: Dept. of Biology, Brown University, Providence, R. I.
Received March 21, 1963.
This article has been cited by other articles:
 |
|
 |
|
  K. L. Becker, E. S. Nylen, J. C. White, B. Muller, and R. H. Snider Jr. Procalcitonin and the Calcitonin Gene Family of Peptides in Inflammation, Infection, and Sepsis: A Journey from Calcitonin Back to Its Precursors J. Clin. Endocrinol. Metab., April 1, 2004; 89(4): 1512 - 1525. [Full Text] [PDF]
|
|
|
|
 |
|
 O. L. Silva and K. L. Becker Salmon Calcitonin in the Treatment of Hypercalcemia Arch Intern Med, September 1, 1973; 132(3): 337 - 339. [Abstract] [PDF]
|
|
|
|
 |
|
 A.W. Fetter and C.C. Capen Ultrastructural Evaluation of Thyroid Parafollicular Cells of Pigs with Naturally Occurring Atrophic Rhinitis Veterinary Pathology, March 1, 1970; 7(2): 171 - 185. [Abstract] [PDF]
|
|
|
|
 |
|
 G. D. AURBACH, J. T. POTTS JR., L. R. CHASE, and G. L. MELSON Polypeptide Hormones and Calcium Metabolism Ann Intern Med, June 1, 1969; 70(6): 1243 - 1265. [Abstract] [PDF]
|
|
|
|
 |
|
 D. H. Copp, D. W. Cockcroft, and Y. Kueh Calcitonin from Ultimobranchial Glands of Dogfish and Chickens Science, November 17, 1967; 158(3803): 924 - 925. [Abstract] [PDF]
|
|
|
|
|
|
P. L. MUNSON Thyrocalcitonin Ann Intern Med, June 1, 1966; 64(6): 1353 - 1357. [Abstract] [PDF]
|
|
|
|
|
|
A. R. ARNSTEIN, B. FRAME, H. M. FROST, and M. A. BLOCK Albright's Hereditary Osteodystrophy: Report of a Family with Studies of Bone Remodeling Ann Intern Med, May 1, 1966; 64(5): 996 - 1008. [Abstract] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
