The present work studied the effects of amiodarone (AMD) and iopanoic acid (IA) on the conversion of thyroxine (T4) to tri-iodothyronine (T3) by rat myocardium. In vivo: male Wistar rats weighing 200-250 g were injected i.p. with AMD (2.5 mg/100 g body weight per day for 12 days) or IA (5 mg/100 g body weight every 12 h for 72 h). Hearts were then removed and processed as in the in-vitro studies. In vitro: hearts were homogenized in Krebs-Ringer phosphate buffer (pH 7.4) and AMD (0.1 mmol/l) or IA (10 mmol/l) plus dithiothreitol (8 mmol/l) and 0.01 microCi [125I]T4 or [125I]T3 were added. After incubation for 2 h at 37 degrees C, radioactive compounds were identified by paper chromatography. Both AMD and IA given in vivo blocked T4 and T3 conversion significantly (P less than 0.005). When added in vitro, AMD failed to inhibit T4 deiodination to T3 whereas IA induced a significant (P less than 0.005) decrease in T3 generation. Deiodination of [125I]T3 by heart homogenates was not altered by AMD or IA. While the expected increase in circulating T4 (P less than 0.001) and decrease in T3 (P less than 0.001) did occur after AMD or IA treatment, plasma TSH in AMD-treated rats was decreased (P less than 0.001), while in IA-treated animals it was increased (P less than 0.001), thus indicating that AMD did not inhibit pituitary type-II 5'-monodeiodinase.(ABSTRACT TRUNCATED AT 250 WORDS)

译文

本工作研究了胺碘酮 (AMD) 和碘酸 (IA) 对大鼠心肌将甲状腺素 (T4) 转化为三碘甲状腺素 (T3) 的影响。体内: i.p.注射体重200-250g的雄性Wistar大鼠。用AMD (每天2.5 mg/100克体重,持续12天) 或IA (每12小时5 mg/100克体重,持续72小时)。然后像体外研究一样取出心脏并进行处理。体外: 将心脏在Krebs-Ringer磷酸盐缓冲液 (pH 7.4) 和AMD (0.1 mmol/l) 或IA (10 mmol/l) 加二硫苏糖醇 (8 mmol/l) 中匀浆,并加入0.01 microCi [125I]T4或 [125I]T3。在37度下孵育2小时后C,放射性化合物通过纸色谱法进行鉴定。AMD和IA在体内均显著阻断了T4和T3的转化 (P小于0.005)。当在体外添加时,AMD未能抑制T4脱碘至T3,而IA诱导T3代显着 (P小于0.005) 减少。心脏匀浆对 [125I]T3的脱碘作用没有被AMD或IA改变。而循环T4的预期增加 (P小于0.001) 和T3的减少 (P小于0.001) 确实发生在AMD或IA治疗后,AMD治疗的大鼠血浆TSH降低 (P小于0.001),而IA治疗的动物血浆TSH升高 (P小于0.001),因此表明AMD没有抑制垂体II型5 '-单脱碘酶。(摘要截短于250字)

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