神经肽Y、钙基因相关肽和P物质在甲状腺中的分布及其在甲亢状态下的变化(英文)

Distribution of NPY,SP,CGRP in rat thyroid and their change under condition of acute experimental hyperthyroidism

以往的研究表明,甲状腺中分布有肽能神经,包括神经肽Y(NPY)能神经、P物质(SP)能神经和脑肠肽(VIP)能神经。这些神经纤维的终末与血管和甲状腺的滤泡接触。一般认为,甲状腺的功能活动主要受下丘脑-垂体-甲状腺轴的调节,有关神经肽的调节,尤其是在甲亢状态下的调节尚不清楚。本研究以SD大鼠为实验动物,通过T4注射建立甲亢动物模型。使用免疫组化技术对NPY、CGRP和SP在实验与对照动物的分布进行形态学研究,使用放射免疫测定技术对模型动物与对照动物甲状腺中的NPY、CGRP和SP进行定量研究。免疫组化技术发现NPY阳性神经纤维密集环绕小血管,其末端与血管内皮紧密联系,一些NPY阳性神经走行于滤泡间的结缔组织中,其末端与滤泡上皮接触;有SP阳性神经纤维走行于滤泡间的结缔组织中,其末端与滤泡上皮接触;CGRP阳性细胞分布于滤泡间的结缔组织中,或滤泡上皮细胞之间。放射免疫测定表明甲亢大鼠NPY、SP水平高于对照大鼠,CGRP水平低于对照大鼠。结果表明,在甲亢状态下,机体通过血管收缩介质NPY、SP的增多与血管舒张介质CGRP的减少,控制甲状腺素进入血液循环,这是机体在病理过程中的自稳机制之一。

Previous work has shown that peptidergic nerve fibers of the thyroid gland contain vasoactive intestinal polypeptide （VIP）, substance P （SP） and neuropeptide Y （NPY）. They contact vessel walls and epithelial cells of follicles and regulate the activity of the smooth muscle and epithelium of the follicle. It is generally accepted that the hypothalamicpituitary -thyroid axis regulates the activity of thyroid follicles. The action of NPY, CGRP and SP, especially in hyperthyroidism, is poorly understood. The acute hyperthyroidism rat model was induced by injection of thyroxine （T4）. NPY, CGRP, SP were tested by RIA. The location and distribution of NPY, CGRP and SP were studied using immunohistochemistry. NPY positive nerve fibers surrounded the small blood vessels, and their terminals contacted endothelial ceils of blood vessels. Some NPY and SP positive nerve fibers were localized in connective tissue between follicles, and their terminals contacted follicular epithelial cells. No CGRP positive nerve fibers were detected. CGRP positive cells were distributed within the epithelium of follicles or adjacent to follicles. Radioimnmnoassay revealed a higher level of NPY and SP in experimental rats following T4 application as compared with control rats, but the level of CGRP was lower than in controls. In hyperthyroidism, increased vasoconstriction caused by increasing of NPY overcomes the weakened vasodilation effects of CGRP decreasing to decrease blood flow and controls T4 into blood circulation. This balance may be considered as one of homeostasis mechanism under process of pathology