Massart C, Hody B, Condé D, Leclech G, Nicol M
Laboratoire de Biochimie A et Service d'O.R.L., C.H.U. de Pontchaillou, Rennes, France.
Mol Cell Endocrinol. 1989 Mar;62(1):113-7. doi: 10.1016/0303-7207(89)90119-6.
Amiodarone and propranolol have been known to inhibit the peripheral conversion of thyroxine (T4) to 3,5,3'-triiodothyronine (T3) but their direct effect on the thyroid gland is not understood. We therefore investigated the action of the two drugs on the functional properties of human thyroid follicles embedded in collagen gel. Amiodarone and propranolol induced a dose-dependent reduction or blocking of the follicular production of cyclic AMP (cAMP), thyroglobulin (Tg) and free triiodothyronine (FT3) under 200 microU/ml medium. Small drug doses and the drug solvents did not affect the follicular secretion. The inhibiting effect of amiodarone and propranolol on follicular production of cAMP, Tg and FT3 appears to result from several factors: (1) inhibition of thyroid 5'-deiodinase; (2) amiodarone high iodine content; (3) a quinidine-like effect of propranolol involving a membrane-stabilizing mechanism.
已知胺碘酮和普萘洛尔可抑制甲状腺素(T4)向3,5,3'-三碘甲状腺原氨酸(T3)的外周转化,但其对甲状腺的直接作用尚不清楚。因此,我们研究了这两种药物对包埋于胶原凝胶中的人甲状腺滤泡功能特性的作用。在200微单位/毫升培养基中,胺碘酮和普萘洛尔可诱导滤泡环磷酸腺苷(cAMP)、甲状腺球蛋白(Tg)和游离三碘甲状腺原氨酸(FT3)生成呈剂量依赖性减少或受阻。小剂量药物及药物溶剂不影响滤泡分泌。胺碘酮和普萘洛尔对滤泡cAMP、Tg和FT3生成的抑制作用似乎源于多种因素:(1)抑制甲状腺5'-脱碘酶;(2)胺碘酮的高碘含量;(3)普萘洛尔类似奎尼丁的作用,涉及膜稳定机制。