Cooke C R, Latif K A, Huch K M, Wall B M
Department of Medicine, Veterans Affairs Medical Center, Memphis, Tenn, 38104, USA.
Am J Nephrol. 1998;18(1):71-6. doi: 10.1159/000013309.
Studies in which plasma osmolality was altered acutely by oral water loading and hypertonic sodium chloride infusion were performed to further identify the mechanisms involved in the pathogenesis of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in a patient with Guillain-Barré syndrome. Although resetting of the osmotic threshold for vasopressin release was demonstrated in these studies, this does not seem to have been a primary factor in the development of SIADH in this patient. Downward resetting of the osmotic threshold by sustained hypoosmolality has been previously demonstrated, and it is possible that this may account for the initially low osmotic threshold identified by our studies. These studies suggest that inappropriate antidiuresis, as shown by the absence of a diuretic response to low threshold suppression of the plasma arginine vasopressin concentration was due either to a vasopressin-independent mechanism or to markedly increased renal tubular sensitivity to vasopressin.
通过口服水负荷和静脉输注高渗氯化钠溶液急性改变血浆渗透压，进行了多项研究，以进一步确定吉兰 - 巴雷综合征患者抗利尿激素分泌不当综合征（SIADH）发病机制中涉及的因素。尽管在这些研究中证实了血管加压素释放的渗透阈值重置，但这似乎并非该患者SIADH发生的主要因素。先前已证实持续低渗可导致渗透阈值向下重置，这可能解释了我们研究中最初发现的低渗透阈值。这些研究表明，如对血浆精氨酸血管加压素浓度低阈值抑制缺乏利尿反应所示，不当抗利尿要么是由于血管加压素非依赖机制，要么是由于肾小管对血管加压素的敏感性显著增加。
