An experimental model of syndrome of inappropriate antidiuretic hormone secretion in the rat.
An experimental model of syndrome of inappropriate antidiuretic hormone secretion in the rat.
复制标题
大鼠抗利尿激素分泌异常综合征的实验模型。
DOI：
10.1152/ajpendo.1984.247.4.e540
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Verbalis,JG
中科院分区：
文献类型：
--
作者：
Verbalis,JG
用精氨酸加压素（AVP）或1-脱氨基-8-D-精氨酸加压素（DDAVP）连续皮下注射清醒无节制饮用5%葡萄糖的大鼠，建立抗利尿激素分泌不当综合征（SIADH）的实验模型。保留摄入的水和内源性产生的游离水从组织catalysts是低钠血症的主要决定因素使用AVP或DDAVP输注。水膨胀后出现短暂性尿钠症，但血浆[Na+]仅略微进一步降低。停止抗利尿剂输注导致游离水排泄，校正血浆[Na+]。低钠血症动物的红细胞体积显著增加，细胞内[K+]和[Na+]均等效降低，与细胞内液被保留水稀释一致。这种SIADH模型与先前描述的模型显著不同，因为在没有高尿流率的情况下不会发生逃避AVP和DDAVP的水渗透作用。使用该模型观察到的结果表明，在SIADH中保留的水主要驻留在细胞内等渗平衡的细胞外液体积。
An experimental model of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) was developed using continuous subcutaneous infusions of arginine vasopressin (AVP) or 1-desamino-8-D-arginine vasopressin (DDAVP) in conscious unrestrained rats drinking 5% dextrose solution. Retention of both ingested water and endogenously generated free water from tissue catabolism was the primary determinant of hyponatremia using either AVP or DDAVP infusions. Natriuresis occurred transiently following water expansion but only slightly further lowered plasma [Na+]. Cessation of antidiuretic infusion resulted in free water excretion with correction of plasma [Na+]. Erythrocyte cell volume was significantly increased in hyponatremic animals and intracellular [K+] and [Na+] both decreased equivalently, consistent with dilution of intracellular fluid by retained water. This model of SIADH differs significantly from those previously described, in that escape from the hydroosmotic effect of AVP and DDAVP does not occur in the absence of high urinary flow rates. The observed results using this model suggest that the retained water in SIADH primarily resides intracellularly following isotonic equilibration of extracellular fluid volume.