喉返神经对大鼠甲状腺摄碘的影响及其机制探讨

（１）切断大鼠单侧喉返神经２、４、２４ｈ后同侧甲状腺摄碘量均明显增高，而在切断单侧喉返神经４ｈ后电刺激其外周端则该侧甲状腺摄碘量较单纯切断神经者减少，事先给以阿托品可阻断电刺激引起的效应。（２）切断大鼠单侧喉返神经１ｄ后，该侧甲状腺滤泡上皮细胞内高尔基复合体是松散状，分泌颗粒增多。（３）切断大鼠单侧喉返神经１０ｄ后，该侧甲状腺滤泡上皮细胞内线粒体明显增多（线粒体体积密度和膜面密度均明显增加）。（４）切断单侧喉返神经或切断后电刺激其外周端所引起的效应在去垂体大鼠仍然出现。（５）切断大鼠单侧喉返神经４ｈ和２４ｈ后，下丘脑内去甲肾上腺素、多巴胺、酪氨酸三种神经递质的含量无明显变化。以上结果表明：喉返神经抑制甲状腺摄碘功能的机制可能是Ｍ受体介导的、纯神经调节作用。

STUDIES ON THE EFFECT AND MECHANISM OF RECURRENT LARYNGEAL NERVE ON THYROIDAL IODINE UPTAKE IN RATS

Homolateral thyroidal radioiodide uptake increased significantly 2,4 and 24 hours after section of unilateral recurrent laryngeal nerve(RLN)after radioiodide injection in rats. When the sectioned peripheral end was stimulated at the 4th hour after radioiodide injection, homolateral thyroidal radioiodide uptake decreased significantly 4 hours after the injection, compared with RLN sectioned group. But the effect of the stimulation could be blocked by atropine used 20 minutes before stimulation.On the 1st day after section of unilateral RLN, loose,secretory vesicles increased in Golgi bodies appeared obviously in the follicular cells of homolateral thyroid.On the 10th day after section of unilateral RLN, volume density and surface density of mitochondria increased significantly,it seemed that endoplasmic reticula increased,lysosomes decreased or disappeared in the follicular cells of homolateral thyroid.Homolateral thyroidal radioiodide uptake increased significantly 4 hours after section of unilateral RLN and radioiedide injection in rats after pituitectomy.When the sectioned peripheral end was stimulated at the 4th hour after radioiodide injection, homolateral thyroidal radioiodide uptake decreased significantly 4 hours after the injection, compared with RLN sectioned rats after pituitectomy.There were no significant variations in norepinephrine(NE),dopamine(DA)and tyrosine(Tyr)in hypothalamus at the 4th,24th hour after section of unilateral RLN,compared with the control group. These results suggest that RLN normally exerts a direct inhibitory effect on thyroidal iodine uptake possibly mediated by muscarinic receptors.