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大鼠双侧蓝斑损毁所致的烦渴症

Hyperdipsia induced by bilateral destruction of the locus coeruleus in rats.

作者信息

Osumi Y, Oishi R, Fujiwara H, Takaori S

出版信息

Brain Res. 1975 Mar 28;86(3):419-27. doi: 10.1016/0006-8993(75)90892-6.

Abstract

Bilateral lesions in the locus coeruleus (LC) of rats induced a urinary disorder and hyperdipsia. Dilatation of the urinary bladder, urinary retention and hematuria with bleeding originating from the urinary bladder, occurred immediately after the lesioning and continued for 2-5 days. Water intake increased 4 days after the lesioning. This hyperdipsia persisted for at least 4 days and then gradually returned to the control level. Food intake decreased for the first 5 days, and then returned to the control level. Lesions in the ascending dorsal bundle (DB) originating from the LC also produced hyperdipsia, but not urinary disorder. Destruction of the ascending ventral vundle (VB) originating from the noradrenaline (NA) neurons in the medulla oblongata did not affect eating, drinking or urination. The LC- or DB-lesioning caused a significant reduction of NA in the whole forebrain except the hypothalamus, whereas VB-lesioning caused reduced NA in the hypothalamus. In LC-lesioned animals, no significant changes were observed in serum osmolarity, Na+, K+, albumin and glucose in serum, or in the excretion of urine in the water-loading test.

摘要

大鼠蓝斑(LC)双侧损伤诱发了排尿障碍和烦渴。损伤后立即出现膀胱扩张、尿潴留以及源自膀胱出血的血尿,并持续2 - 5天。损伤后4天饮水量增加。这种烦渴持续至少4天,然后逐渐恢复到对照水平。最初5天食物摄入量减少,然后恢复到对照水平。源自LC的背侧上行束(DB)损伤也产生烦渴,但不引起排尿障碍。源自延髓去甲肾上腺素(NA)神经元的腹侧上行束(VB)破坏不影响进食、饮水或排尿。LC或DB损伤导致除下丘脑外的整个前脑NA显著减少,而VB损伤导致下丘脑NA减少。在LC损伤的动物中,血清渗透压、血清中的Na⁺、K⁺、白蛋白和葡萄糖,或水负荷试验中的尿排泄均未观察到显著变化。

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