前言尿崩症(Diabetes insipidus)是后(神经)脑垂体机能减退致使抗利尿激素分泌过少所引起之综合征。临床表现以烦喝多尿、尿比重固定低,尿糖阴性而无肾功能变异。远在1925年 Starling 及 Verney 二氏应用离体肾脏来研究此症。1927年及二氏实验证明尿崩症具有神经反射性之推论。嗣后有关此症动物研究材料陆续可见。Brooks 氏的实验报告,将猴的脑下垂体与下视丘切断则出现肥胖症及性行为紊乱,同时发生多尿症。 Introduction Diabetes insipidus is a syndrome caused by hypopigmentation of the posterior (nerve) pituitary dysfunction. Clinical manifestations to annoying polyuria, fixed urinary specific low urine negative without renal function variability. Starling and Verney II used isolated kidneys far in 1925 to study the condition. In 1927 and two experiments proved that diabetes insipidus reflex neurological inference. Later on the disease animal research materials one after another. Brooks’s experimental report, the monkey’s pituitary gland cut off with the lower hypothalamus appears obesity and sexual disorders, with polyuria.