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促甲状腺激素对甲状腺血管传导性的影响。

Effects of thyrotropin on the vascular conductance of the thyroid gland.

作者信息

Connors J M, Huffman L J, Hedge G A

机构信息

Department of Physiology, West Virginia University Medical Center, Morgantown 26506.

出版信息

Endocrinology. 1988 Mar;122(3):921-9. doi: 10.1210/endo-122-3-921.

Abstract

It is well established that TSH from the anterior pituitary is the principal stimulatory agent in the physiological regulation of the thyroid gland. Chronic elevations of plasma TSH induce hyperplasia and hypertrophy of thyroid follicular cells and enlargement of blood capillaries. At low plasma TSH levels the thyroid gland atrophies. We have examined the vascular conductance (C = blood flow/mean arterial pressure) of the thyroid gland and several other tissues over a wide range of endogenous plasma TSH concentrations and after treatment with bovine TSH (bTSH) in rats. Tissue blood flows were determined using 15 +/- 5-microns diameter 141Ce-labeled microspheres in a modification of the reference sample microsphere technique. The microspheres were injected directly into the left cardiac ventricle via a 23-gauge needle passed through the chest wall, while the reference blood sample was collected and systemic arterial blood pressure was monitored through femoral arterial catheters. After the animals were killed, tissues were cleaned and weighed, and the tissue radioactivity was determined. Blood samples for determination of plasma hormone levels were obtained from the jugular vein before the injection of microspheres. In the first series of experiments, the vascular C per mass of thyroid gland was significantly decreased 4 and 8 days after hypophysectomy. Treatment of hypophysectomized rats with bTSH (185 mU/100 g.day as a continuous iv infusion for 2 or 6 days) restored thyroid vascular C per mass of tissue to control levels. In the second series of experiments, we manipulated circulating plasma TSH levels in intact rats by 6 days of treatment with propylthiouracil (2.0 mg/day, ip), thyroid hormones (1.5 micrograms T4, 0.4 micrograms T3 or 3.0 micrograms T4, plus 0.8 micrograms T3/100 g.day, sc by continuous infusion), TRH (240 micrograms/day, iv, by continuous infusion), bTSH (800 mU/day, iv, by continuous infusion), or combinations of these treatments. The vascular C per mass of thyroid gland was significantly decreased at very low chronic plasma TSH levels and increased at very high chronic plasma TSH levels. Thyroid vascular C per mass was unchanged, however, over a broad intermediate range of plasma TSH concentrations encompassing normal values, despite alterations in the size and function of the thyroid gland. At these intermediate levels of TSH stimulation, the thyroid gland may respond by adding or subtracting functional units without changing the blood flow per unit. The amount of blood flow per functional unit may be altered only at very high or very low levels of TSH stimulation.

摘要

垂体前叶分泌的促甲状腺激素(TSH)是甲状腺生理调节中的主要刺激因子,这一点已得到充分证实。血浆TSH的长期升高会导致甲状腺滤泡细胞增生和肥大以及毛细血管扩张。血浆TSH水平较低时,甲状腺会萎缩。我们在大鼠体内广泛的内源性血浆TSH浓度范围内,以及在用牛TSH(bTSH)治疗后,检测了甲状腺及其他几种组织的血管传导率(C = 血流量/平均动脉压)。采用改良的参考样本微球技术,使用直径为15±5微米的141Ce标记微球测定组织血流量。微球通过一根穿过胸壁的23号针头直接注入左心室,同时采集参考血样,并通过股动脉导管监测全身动脉血压。动物处死后,清理并称重组织,测定组织放射性。在注射微球前,从颈静脉采集血样以测定血浆激素水平。在第一系列实验中,垂体切除术后4天和8天,每克甲状腺的血管传导率显著降低。用bTSH(185 mU/100 g·天,连续静脉输注2天或6天)治疗垂体切除的大鼠,可使每克组织的甲状腺血管传导率恢复至对照水平。在第二系列实验中,我们通过用丙硫氧嘧啶(2.0 mg/天,腹腔注射)、甲状腺激素(1.5微克T4、0.4微克T3或3.0微克T4加0.8微克T3/100 g·天,皮下连续输注)、促甲状腺激素释放激素(TRH,240微克/天,静脉连续输注)、bTSH(800 mU/天,静脉连续输注)或这些治疗的组合对完整大鼠进行6天治疗,来调节循环血浆TSH水平。在慢性血浆TSH水平非常低时,每克甲状腺的血管传导率显著降低,而在慢性血浆TSH水平非常高时则升高。然而,在包括正常值在内的广泛的血浆TSH浓度中间范围内,尽管甲状腺的大小和功能发生了改变,但每克甲状腺的血管传导率并未改变。在这些TSH刺激的中间水平,甲状腺可能通过增加或减少功能单位来做出反应,而不会改变单位血流量。仅在TSH刺激的非常高或非常低水平时,每个功能单位的血流量才可能发生改变。

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