阿霉素肾病大鼠肾钠潴留机制的初步研究

PRELIMINARY STUDY ON MECHANISMOF SODIUM AND WATER RETENTION IN NEPHROTIC SYNDROME IN RATS INDUCEDBY ADRIAMYCIN

在大鼠阿霉素肾病模型，利用血小板活化因子拮抗剂对蛋白尿的保护作用，研究肾钠潴留与尿蛋白的关系；并测定肾组织匀浆中钠－钾－三磷酸腺甙酶的活性，证实了肾病时肾钠潴留与尿蛋白无关。从而提出本模型中肾钠潴留系阿霉素对小管细胞的直接作用所致，肾内因素为小管细胞钠－钾－三磷酸腺甙酶活性的增高，潴留部位在内髓集合管的假说。

AbstractUsing the model of adriamycin-inducednephrotic syndrome in rats,we studied the relationshipbetween the renal sodium retention effect andproteinuria and determined the activity ofNa￣+-K￣+-ATPase in renal tissue homogenate ofnephrotic rats.No relationship was found between theincreased sodium-water reabsooption and proteinuria.But the impaired salt excretion was related to the in-crease of Na￣+-K￣+-ATPase activity in the renal innermedulla.We propose that direct effects of adriamycinon renal tubule cells are the primary events,that theincreased Na￣+-K￣+-ATPase activity on basolateralmembrane of renal tubule cells is an intrarenal factorwhich mediatcs the retention of salt and water by thekidney and that inner medullary collecting ducts maybe one of the sites of the sodium retention in nephroticrats.