11-脱氧皮质酮引起的高血压、肾小球硬化和肾动脉、小动脉病变。

T Shimamura
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引用次数: 0

摘要

研究了11-脱氧皮质酮和盐负荷对大鼠肾小球硬化和血管病变的影响。肾小球病变开始为局灶性节段性硬化。全局硬化的肾小球体积增大,表明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变无关。动脉系统未见明显的结构改变。总之,doc -盐诱导的肾小球硬化以节段性病变开始,独立于肾小球前小动脉的结构改变而发生,并且没有肾内动脉狭窄的证据。血流动力学应激相关的肾小球微循环系统损伤是doc - salt诱导肾小球硬化的主要原因,需要进一步的研究来阐明其作用。
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11-Deoxycorticosterone-induced hypertension, glomerulosclerosis and renal arterial and arteriolar lesions.

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.

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