采用盐酸和胶原酶消化动脉外膜的技术,对正常的脑动脉、蛛网膜下腔出血后痉挛的脑动脉及经前列腺素F2α(prostaglandin F2α,PGF2α)处理的脑动脉平滑肌细胞构筑进行研究。结果显示:正常平滑肌细胞是梭形的,沿着血管长轴环行分布,细胞间通过突起相连,肌细胞外膜面通常是光滑的;痉挛的脑动脉和经PGF2α处理的脑动脉平滑肌外膜面均出现非常相似的膜皱折和卷曲,肌间隙增宽。透射电镜显示急性痉挛管壁病理变化轻微;迟发性痉挛出现明显病理性超微结构改变。实验结果提示急性脑血管痉挛是由平滑肌收缩引起,病理变化轻微;迟发性脑血管痉挛是血管持久收缩伴病理性超微结构改变。 The arterial adventitial membrane was digested by hydrochloric acid and collagenase. The normal cerebral arteries, cerebral arteries after spasm of subarachnoid hemorrhage and the construction of smooth muscle cells of cerebral artery treated by prostaglandin F2α (PGF2α) were studied. The results showed that the normal smooth muscle cells were fusiform and circled along the long axis of blood vessels. The intercellular connections were made by protrusions. The outer membrane surface of muscle cells was usually smooth. The spastic cerebral arteries and PGF2α-treated smooth muscle surface of cerebral arteries Very similar membrane wrinkles and curls appeared, and the muscle space was widened. Transmission electron microscopy showed mild spasm pathological changes in the wall; delayed spasm obvious pathological ultrastructural changes. Experimental results suggest that acute cerebral vasospasm caused by smooth muscle contraction, pathological changes slightly; delayed cerebral vasospasm is persistent vasoconstriction with pathological ultrastructural changes.