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Parathyroid Ablation in Dystrophic Hamsters: EFFECTS ON CA CONTENT AND HISTOLOGY OF HEART, DIAPHRAGM, AND RECTUS FEMORIS
Genaro M. A. Palmieri, … , Tulio E. Bertorini, James C. Williams
Genaro M. A. Palmieri, … , Tulio E. Bertorini, James C. Williams
Published September 1, 1981
Citation Information: J Clin Invest. 1981;68(3):646-654. https://doi.org/10.1172/JCI110299.
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Parathyroid Ablation in Dystrophic Hamsters: EFFECTS ON CA CONTENT AND HISTOLOGY OF HEART, DIAPHRAGM, AND RECTUS FEMORIS

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Abstract

Cumulative evidence indicates that there is an increased accumulation of calcium in dystrophic muscle and that this may have a pathophysiological role in the progression of the dystrophic process. The accumulation may be related to a defect of the plasma membrane. Because parathyroid hormone (PTH) stimulates calcium influx into the cytosol, the chronic effects of surgical ablation of the parathyroid glands on muscle Ca, Mg, protein synthesis, and histology, as well as plasma creatine phosphokinase (CPK), Ca, and Mg, were studied in normal and dystrophic (BIO 14.6) hamsters. Thyroparathyroidectomized (TPTX) hamsters receiving replacement doses of l-thyroxine were killed at age 90 d, 55 d after TPTX. In intact dystrophic hamsters, the Ca content in the heart was 20 times higher than in normal animals and was reduced by half in TPTX dystrophic hamsters. Similar results were observed in diaphragm and rectus femoris. No abnormalities in Mg content were observed in intact or TPTX dystrophic hamsters. Ether-extractable fat of the heart and diaphragm was reduced in dystrophic hamsters and was not modified by TPTX. Protein synthesis was enhanced in the diaphragm of dystrophic hamsters but was not changed by TPTX. The concentration of CPK in plasma was elevated in dystrophic hamsters and fell significantly after TPTX. In the latter animals, microscopic examination of the heart showed lesser signs of dystrophy, particularly in the degree of fibrosis.

Authors

Genaro M. A. Palmieri, David F. Nutting, Syamal K. Bhattacharya, Tulio E. Bertorini, James C. Williams

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