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用酶组织化学方法观察了自发性高血压大鼠（ＳＨＲ）和正常血压的ＳＤ大鼠在脑梗塞后缺血区的皮质微血管壁，以探讨大脑中动脉（ｍｉｄｄｌｅｃｅｒｅｂｒａｌａｒｔｅｒｙ，ＭＣＡ）阻断后梗塞区脑血管壁的代谢情况，结果显示，缺血１５ｍｉｎ，脑梗塞区血管壁的细胞色素Ｃ氧化酶（ＣＣＯ）和球肌蛋白ＡＴＰ酶（ｍｙｏｓｉｎＡＴＰａｓｅ）活性降低，乳酸脱氢酶（ＬＤＨ）的活性增强。随缺血时间延长，与ＳＤ大鼠相比较，ＳＨＲ脑血管壁的上述变化更为明显，提示ＳＨＲ脑血管壁对缺血具有高度的敏感性。
The cortical microvessel wall in the ischemic area of spontaneous hypertensive rats (SHR) and normotensive SD rats was observed by enzymatic histochemical method to explore the relationship between cerebral infarction (MCA) infarction area and middle cerebral artery occlusion The results showed that the activity of cytochrome C oxidase (CCO) and myosin ATPase (ATPase) in the vascular wall of cerebral infarction area decreased and the activity of lactate dehydrogenase (LDH) increased . With the prolongation of ischemia, compared with SD rats, the changes of SHR in the cerebrovascular wall were more obvious, suggesting that SHR cerebrovascular wall is highly sensitive to ischemia.