Shimamura T
Department of Pathology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway 08854.
Jpn J Exp Med. 1988 Oct;58(5):225-8.
Glomerulosclerosis and vascular lesions occurring in rats receiving 11-deoxycorticosterone and salt-loading have been studied in order to examine their relationship. The glomerular lesion started as focal segmental sclerosis. The globally sclerosed glomeruli were enlarged in size, demonstrating that these showed no evidence of ischemic atrophy. Advanced glomerulosclerosis occurred independent of preglomerular arteriolar pathologic lesion. No meaningful structural changes were observed in the arterial system. In conclusion, DOC-salt-induced glomerulosclerosis started as segmental lesion, occurred independent of structural alterations in the preglomerular arterioles, and took place without evidence of intrarenal arterial stenosis. Further studies are necessary to clarify about the role of hemodynamic stress-related injury to glomerular microcirculatory system as a major cause for DOC-Salt-induced glomerulosclerosis.
为了研究它们之间的关系，对接受11-脱氧皮质酮和高盐饮食的大鼠所出现的肾小球硬化和血管病变进行了研究。肾小球病变始于局灶节段性硬化。全球硬化的肾小球体积增大，表明这些肾小球没有缺血性萎缩的迹象。晚期肾小球硬化的发生与肾小球前小动脉病理病变无关。在动脉系统中未观察到有意义的结构变化。总之，脱氧皮质酮-高盐诱导的肾小球硬化始于节段性病变，其发生与肾小球前小动脉的结构改变无关，且发生时没有肾内动脉狭窄的证据。有必要进行进一步研究，以阐明血流动力学应激相关损伤对肾小球微循环系统的作用，这是脱氧皮质酮-高盐诱导的肾小球硬化的主要原因。
