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对碘缺乏大鼠急性或慢性给予碘化物后血浆促甲状腺激素、甲状腺素和三碘甲状腺原氨酸的变化。

Changes in plasma thyrotrophin, thyroxine, and triiodothyronine after acute or chronic administration of iodide to iodine-deficient rats.

作者信息

Fukuda H, Yasuda N, Greer M A

出版信息

Endocrinology. 1975 Nov;97(5):1196-204. doi: 10.1210/endo-97-5-1196.

Abstract

The effect of chronic oral or acute iv administration of small graded doses of iodide was studied in severely iodine-deficient rats. Drinking water supplemented with 0.1, 0.2, or 0.4 mug 127I-/ml was given for up to 42 days. Plasma T3, which was initially in the normal range, increased 2--3-fold on days 1 and 2 after initiation of iodide supplementation, then dropped to approximately the intial concentration at day 3. Plasma T4, initially undetectable, was calculated to increase approximately 20-fold within one day after beginning iodide supplementation, but was still climbing into the normal range at day 3. In all groups, the initially high plasma TSH fell significantly by day 1 and was in approximately the normal range for iodine-sufficient rats by day 3. At 42 days, thyroid weight and 131I uptake were significantly elevated in all groups and inversely correlated with the dose of iodide, even though the thyroidal labeled T3/T4 ratio and plasma TSH, T4, and T3 were within the normal range. Intravenous injection of 0.1 or 0.5 mug 125I-/100 g caused an approximately 2-fold increase in plasma T3 within 24 h, which was not statistically different between the 2 groups. Plasma T4 rose to the normal range 24 h after 0.5 mug and was slightly, but significantly, elevated after 0.1 mug; it then declined in both groups. Twenty-four hours after injection of 2.5 mug 125I-/100 g, there was a significant fall in plasma T3, no change in plasma TSH, and no detectable plasma T4. Thereafter, there was a dramatic increase in plasma T4 and a fall in plasma TSH. The duration and degree of suppression of plasma TSH was related to the dose of iodide injected. We conclude that, under the conditions of our experiments, plasma T3 derives primarily from thyroidal secretion rather than from extra-thyroidal conversion of T4 to T3. Severely iodine-deficient rats secrete maximum quantities of TSH which are not increased by a further transient drop in plasma thyroid hormone concentration.

摘要

在严重缺碘的大鼠中研究了小剂量分级碘化钾长期口服或急性静脉注射的效果。给大鼠饮用补充了0.1、0.2或0.4μg 127I⁻/ml的饮用水,持续42天。血浆T3最初在正常范围内,在补充碘化物开始后的第1天和第2天增加了2 - 3倍,然后在第3天降至大约初始浓度。血浆T4最初检测不到,在开始补充碘化物后的一天内计算增加了约20倍,但在第3天仍在攀升至正常范围。在所有组中,最初较高的血浆促甲状腺激素(TSH)在第1天显著下降,到第3天已大致处于碘充足大鼠的正常范围内。在42天时,所有组的甲状腺重量和131I摄取量均显著升高,且与碘化物剂量呈负相关,尽管甲状腺标记的T3/T4比值以及血浆TSH、T4和T3均在正常范围内。静脉注射0.1或0.5μg 125I⁻/100g在24小时内使血浆T3增加约2倍,两组之间无统计学差异。0.5μg注射后24小时血浆T4升至正常范围,0.1μg注射后略有但显著升高;然后两组均下降。注射2.5μg 125I⁻/100g后24小时,血浆T3显著下降,血浆TSH无变化,血浆T4检测不到。此后,血浆T4急剧增加,血浆TSH下降。血浆TSH抑制的持续时间和程度与注射的碘化物剂量有关。我们得出结论,在我们的实验条件下,血浆T3主要来源于甲状腺分泌,而非T4的甲状腺外转化为T3。严重缺碘的大鼠分泌最大量的TSH,血浆甲状腺激素浓度的进一步短暂下降不会使其增加。

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