Thompson C J, Baylis P H
Endocrine Unit, Royal Victoria Infirmary, Newcastle upon Tyne.
Q J Med. 1987 Oct;65(246):853-62.
Patients with cranial diabetes insipidus are unable to concentrate urine, and depend on thirst and water intake to prevent hypertonic dehydration. Using a visual analogue scale (0-10 cm) we studied osmotically stimulated thirst induced by hypertonic saline infusion in 15 patients with diabetes insipidus and 15 healthy controls. Plasma osmolality in the patients rose from 292 +/- 1 to 316 +/- 1 mOsm/kg (p less than 0.001), and 13 patients showed a progressive rise in thirst ratings (1.4 +/- 0.4 to 8.1 +/- 0.3 cm, p less than 0.001) with abolition of thirst by drinking, in a similar fashion to controls. Water intake following infusion was greater in patients than controls (p less than 0.001). Linear regression analysis of thirst and plasma osmolality showed no difference in the osmotic threshold for thirst onset, or the sensitivity of thirst osmoreceptors, between 13 of the patients and the control group. One patient was shown to be hypodipsic and compulsive water drinking was demonstrated in another: abnormal thirst perception caused abnormalities of salt and water balance in these two patients. Most patients with cranial diabetes insipidus have normal thirst mechanisms, though clinically significant hypodipsia or hyperdipsia may co-exist with vasopressin deficiency.
颅咽管型尿崩症患者无法浓缩尿液，需依靠口渴感和饮水来预防高渗性脱水。我们使用视觉模拟量表（0 - 10厘米），研究了15例尿崩症患者和15名健康对照者在静脉输注高渗盐水后，由渗透压刺激引起的口渴情况。患者的血浆渗透压从292±1毫摩尔/千克升至316±1毫摩尔/千克（p＜0.001），13例患者的口渴评分逐渐升高（从1.4±0.4厘米升至8.1±0.3厘米，p＜0.001），饮水后口渴缓解，这一情况与对照组相似。输注后患者的饮水量高于对照组（p＜0.001）。对13例患者和对照组的口渴感与血浆渗透压进行线性回归分析，结果显示口渴起始的渗透压阈值或口渴渗透压感受器的敏感性并无差异。有1例患者表现为口渴减退，另1例则出现强迫性饮水：这两名患者的口渴感知异常导致了水盐平衡紊乱。大多数颅咽管型尿崩症患者的口渴机制正常，不过临床上显著的口渴减退或亢进可能与抗利尿激素缺乏并存。
