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BioMed Research International
Volume 2017, Article ID 6071031, 11 pages
Research Article

Recovery following Thyroxine Treatment Withdrawal, but Not Propylthiouracil, Averts In Vivo and Ex Vivo Thyroxine-Provoked Cardiac Complications in Adult FVB/N Mice

1Department of Physiology and Cell Biology, College of Medicine, The Ohio State University, Columbus, OH, USA
2Dorothy M. Davis Heart & Lung Research Institute, The Ohio State University, Columbus, OH, USA
3Department of Pharmacology and Toxicology, Faculty of Pharmacy, Helwan University, Cairo, Egypt

Correspondence should be addressed to Paul M. L. Janssen; ude.uso@01.nessnaj and Mohammad T. Elnakish; ude.uso@1.hsikanle

Received 20 March 2017; Revised 5 June 2017; Accepted 8 June 2017; Published 16 July 2017

Academic Editor: Natale Daniele Brunetti

Copyright © 2017 Nancy S. Saad et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Persistent cardiovascular pathology has been described in hyperthyroid patients even with effective antithyroid treatment. Here, we studied the effect of a well-known antithyroid drug, propylthiouracil (PTU; 20 mg/kg/day), on thyroxine (T4; 500 µg/kg/day)-induced increase in blood pressure (BP), cardiac hypertrophy, and altered responses of the contractile myocardium both in vivo and ex vivo after 2 weeks of treatment. Furthermore, the potential recovery through 2 weeks of T4 treatment discontinuation was also investigated. PTU and T4 recovery partially reduced the T4-prompted increase in BP. Alternatively, PTU significantly improved the in vivo left ventricular (LV) function with no considerable effects on cardiac hypertrophy or ex vivo right ventricular (RV) contractile alterations subsequent to T4 treatment. Conversely, T4 recovery considerably enhanced the T4-provoked cardiac changes both in vivo and ex vivo. Altogether, our data is in agreement with the proposal that hyperthyroidism-induced cardiovascular pathology could persevere even with antithyroid treatments, such as PTU. However, this cannot be generalized and further investigation with different antithyroid treatments should be executed. Moreover, we reveal that recovery following experimental hyperthyroidism could potentially ameliorate cardiac function and decrease the risk for additional cardiac complications, yet, this appears to be model-dependent and should be cautiously construed.