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Thyroid Function Disturbance and Type 3 Iodothyronine Deiodinase Induction after Myocardial Infarction in Rats—A Time Course Study

Departamento de Ciências Fisiológicas (E.L.O., R.H.C.S., I.G.A.), Instituto de Biologia, Universidade Federal Rural do Rio de Janeiro, CEP 23890-000, Seropédica, Rio de Janeiro, Brazil; Fundação Centro de Educação Superior a Distância do Estado do Rio de Janeiro (M.O.M.), Ecodata Exames Médicos LTDA (E.C.M.), Laboratórios de Fisiologia Endócrina (M.P.M., R.S.F., A.C.M.S., D.P.C.) and Laboratório Endocrinologia Molecular (R.H.C.S.), Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Centro de Ciências da Saúde, Bloco G, Ilha do Fundão, CEP 21949-900 Rio de Janeiro, Brazil; and Division of Endocrinology, Diabetes, and Hypertension (M.A.M., S.A.H., A.C.B.), Department of Medicine, Brigham and Women’s Hospital, Boston, Massachusetts 02115

Address all correspondence and requests for reprints to: Emerson Lopes Olivares, D.V.M., M.Sc., D.Sc., Departamento de Ciências Fisiológicas, Instituto de Biologia, Universidade Federal Rural do Rio de Janeiro BR 465, Km 7, 23851-000, Seropédica, Rio de Janeiro, Brazil. E-mail: elopes{at}ufrrj.br.

In humans, there is a significant decrease in serum T₃ and increase in rT₃ at different time points after myocardial infarction, whereas serum TSH and T₄ remain unaltered. We report here a time course study of pituitary-thyroid function and thyroid hormone metabolism in rats subjected to myocardial infarction by left coronary ligation (INF). INF- and sham-operated animals were followed by serial deiodination assays and thyroid function tests, just before, and 1, 4, 8, and 12 wk after surgery. At 4 and 12 wk after INF, liver type 1 deiodinase activity was significantly lower, confirming tissue hypothyroidism. Type 3 deiodinase (D3) activity was robustly induced 1 wk after INF only in the infarcted myocardium. Reminiscent of the consumptive hypothyroidism observed in patients with large D3-expressing tumors, this induction of cardiac D3 activity was associated with a decrease in both serum T₄ (50% decrease) and T₃ (37% decrease), despite compensatory stimulation of the thyroid. Thyroid stimulation was documented by both hyperthyrotropinemia and radioiodine uptake. Serum TSH increased by 4.3-fold in the first and 3.1-fold in the fourth weeks (P < 0.01), returning to the basal levels thereafter. Thyroid sodium/iodide-symporter function increased 1 wk after INF, accompanying the increased serum TSH. We conclude that the acute decrease in serum T₄ and T₃ after INF is due to increased thyroid hormone catabolism from ectopic D3 expression in the heart.

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