Christensen S
Scand J Clin Lab Invest. 1980 Apr;40(2):151-7. doi: 10.3109/00365518009093018.
The antidiuretic responses of arginine vasopressin (AVP) and 1-desamino-8-D-arginine vasopressin (DDAVP) were studied in rats with marked lithium-polyuria (about 100 ml/100 g/24 h) induced by administration of lithium to the diet for 3-4 months. The hormones were infused i.v. and s.c. at a constant rate for 7 days using implantable osmotic minipumps. Body weight, food consumption and urine volume and osmolality were recorded daily. Whereas supramaximal doses of AVP only had little effect on spontaneous urine flow and osmolality, DDAVP (0.1 microgram/h i.v. or 1 microgram/H s.c.) restored urine volume and osmolality to near-normal values. Although the mechanism of the antidiuresis evoked by DDAVP was not investigated the ability of this compound to reverse AVP-resistant polyuria may be due to its specificity and high intrinsic activity in stimulating the vasopressin receptor. The reversibility of lithium-induced impairment of renal concentrating ability caused by excessive hormonal stimulation is not immediately compatible with the recent hypothesis that lithium-polyuria may reflect irreversible structural kidney damage.
在通过在饮食中给予锂3 - 4个月诱导出显著锂性多尿(约100 ml/100 g/24 h)的大鼠中,研究了精氨酸加压素(AVP)和1 - 去氨基 - 8 - D - 精氨酸加压素(DDAVP)的抗利尿反应。使用可植入式渗透微型泵以恒定速率静脉内和皮下输注这些激素7天。每天记录体重、食物摄入量、尿量和渗透压。虽然超最大剂量的AVP对自发尿量和渗透压几乎没有影响,但DDAVP(静脉内0.1微克/小时或皮下1微克/小时)可使尿量和渗透压恢复到接近正常的值。尽管未研究DDAVP引起抗利尿作用的机制,但该化合物逆转AVP抵抗性多尿的能力可能归因于其在刺激加压素受体方面的特异性和高内在活性。由过度激素刺激导致的锂诱导肾浓缩能力损害的可逆性与最近关于锂性多尿可能反映不可逆肾脏结构损伤的假说并不立即相符。