Lin J X, Tomimoto H, Akiguchi I, Wakita H, Shibasaki H, Horie R
Department of Neurology, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8507, Japan.
Neuroreport. 2001 Jul 3;12(9):1835-9. doi: 10.1097/00001756-200107030-00015.
There have been few studies on the white matter lesions of spontaneously hypertensive rats (SHR). From the point of view of hypertension and arteriosclerosis, white matter lesions were examined in SHR and stroke-prone SHR (SHRSP), and were then compared with Wistar-Kyoto (WKY) rats. The vasculopathy was analyzed by morphometric immunohistochemistry for collagen and smooth muscle actin. Both SHR and SHRSP had hypertension at > or = 12 weeks of age, and the latter developed severe white matter lesions at 20 weeks. Immuno- histochemistry revealed proliferation of microglia in the white matter and an increase in smooth muscle actin in the vessels of SHRSP compared with the WKY rats and SHR, but there were no changes in the collagen. These results indicate a role of hypertension in the pathogenesis of white matter lesions. However, genetic difference may also be responsible since SHR and SHRSP showed similar hypertension.
关于自发性高血压大鼠（SHR）白质病变的研究较少。从高血压和动脉硬化的角度出发，对SHR和易中风SHR（SHRSP）的白质病变进行了检查，然后与Wistar-Kyoto（WKY）大鼠进行比较。通过对胶原蛋白和平滑肌肌动蛋白进行形态计量免疫组织化学分析血管病变。SHR和SHRSP在12周龄及以上时均患有高血压，后者在20周时出现严重的白质病变。免疫组织化学显示，与WKY大鼠和SHR相比，SHRSP白质中的小胶质细胞增殖，血管中的平滑肌肌动蛋白增加，但胶原蛋白没有变化。这些结果表明高血压在白质病变发病机制中起作用。然而，遗传差异也可能是原因之一，因为SHR和SHRSP表现出相似的高血压。
