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脑动脉壁中膜平滑肌细胞（ＳＭＣ）的改变是高血压诱发脑卒中的病理基础。本文用透射电镜观察了易卒中型肾血管性高血压大鼠（ＲＨＲＳＰ）基底动脉超微结构的变化，并用体视学方法对基底动脉中膜平滑肌层面积与中膜总面积之比作动态定量分析。①透射电镜观察：高血压组７ｄ内弹力膜（ＩＥＬ）增厚，中膜ＳＭＣ略有肥大；３０ｄ内皮细胞伸出伪足穿透ＩＥＬ，中膜ＳＭＣ胞体增大，细胞间隙变宽，间质增多；９０ｄＳＭＣ排列紊乱，细胞变性、坏死，失去正常形态，残余胞质内可见大量粗面内织网（ＲＥＲ），细胞间隙增宽，充满间质，其中有大量ＳＭＣ坏死碎片。②透射电镜定量分析：高血压组基底动脉中膜平滑肌层面积与中膜总面积之比７ｄ、３０ｄ无明显改变；９０ｄ较对照组及高血压组７ｄ、３０ｄ显著减少（Ｐ＜０．０１）。提示：脑血管ＳＭＣ外间质成份增多、ＳＭＣ大量变性坏死所致中膜ＳＭＣ面积降低可能与高血压晚期发生脑卒中有关。
The change of SMC in the arterial wall is the pathological basis of hypertension-induced stroke. In this paper, the ultrastructure of basilar artery of the rat with stroke-induced renovascular hypertension (RHRSP) was observed by transmission electron microscopy. The ratio of the basilar artery medial smooth muscle area to the total area of the tunica media was dynamically determined by stereological method analysis. ① Transmission electron microscopy: hypertensive group 7d inner elastic membrane (IEL) thickened, a slight hypertrophy of the media SMC; 30d endothelial cells extending pseudopodia penetrate IEL, SMC cell mass in the media, cell gap widening, interstitial Increased 90 dSMC disorganized, cell degeneration, necrosis, lost the normal morphology, the residual cytoplasm can be seen in a large number of rough inner network (RER), the cell gap widened, filled with stroma, including a large number of SMC necrotic fragments. (2) Quantitative analysis by transmission electron microscopy: there was no significant change in the ratio of basilar artery medial smooth muscle area to medial area in 7d and 30d in hypertensive group, and decreased significantly in 90d compared with control group and hypertension group (P <0.01) . Prompted: cerebrovascular SMC increased interstitial components, a large number of SMC degeneration and necrosis caused by reduced area of the media in the SMC may be associated with late onset of stroke in stroke.