Olivares Emerson L, Marassi Michelle P, Fortunato Rodrigo S, da Silva Alba C M, Costa-e-Sousa Ricardo H, Araújo Iracema G, Mattos Elisabete C, Masuda Masako O, Mulcahey Michelle A, Huang Stephen A, Bianco Antonio C, Carvalho Denise P
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.
Endocrinology. 2007 Oct;148(10):4786-92. doi: 10.1210/en.2007-0043. Epub 2007 Jul 12.
In humans, there is a significant decrease in serum T(3) and increase in rT(3) at different time points after myocardial infarction, whereas serum TSH and T(4) 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 T(4) ( approximately 50% decrease) and T(3) (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 T(4) and T(3) after INF is due to increased thyroid hormone catabolism from ectopic D3 expression in the heart.
在人类中，心肌梗死后不同时间点血清T(3)显著降低，反T(3)升高，而血清促甲状腺激素(TSH)和T(4)保持不变。我们在此报告一项对通过左冠状动脉结扎(INF)诱导心肌梗死的大鼠垂体-甲状腺功能和甲状腺激素代谢的时间进程研究。对INF组和假手术组动物在手术前以及术后1、4、8和12周进行连续的脱碘测定和甲状腺功能测试。INF术后4周和12周，肝脏1型脱碘酶活性显著降低，证实存在组织甲状腺功能减退。3型脱碘酶(D3)活性仅在INF术后1周在梗死心肌中被强烈诱导。这类似于在表达大量D3的肿瘤患者中观察到的消耗性甲状腺功能减退，尽管甲状腺受到代偿性刺激，但心脏D3活性的这种诱导与血清T(4)(约降低50%)和T(3)(降低37%)的降低有关。甲状腺刺激通过高促甲状腺激素血症和放射性碘摄取得以证实。血清TSH在第一周增加4.3倍，第四周增加3.1倍(P<0.01)，此后恢复到基础水平。甲状腺钠/碘同向转运体功能在INF术后1周增加，与血清TSH升高同时出现。我们得出结论，INF术后血清T(4)和T(3)的急性降低是由于心脏中异位D3表达导致甲状腺激素分解代谢增加。
