Abstract: Objective To explore the mechanism of delayed cerebral ischemia after subarachnoid hemorrhage (SAH), in order to find out new therapy to improve the prevention and treatment of cerebral ischemia after SAH. Methods SAH model was established by trans-carotid puncture of intracranial artery with nylon suture. The experimental mice were divided into sham group (n = 5) and 24 h, 48 h, 72 h after SAH groups, namely 24 h group (n = 4), 48 h group (n = 6) and 72 h group (n = 8). SAH was diagnosed by gross specimen and histological examination but not by the presentation of intracerebral hemorrhage. Intracerebral microemboli were identified by immunohistochemical fluorescent. The mean number of microemboli per mm2 (microemboli burden) was calculated and compared in different groups. Results Microemboli appeared in cluster, and were scattered equally throughout both hemispheres. The number of microemboli were 0.00 (0.00, 0.05)/mm2 in sham group, 0.29 (0.11, 0.46)/mm2 in 24 h group, 2.30 (1.24, 3.87)/mm2 in 48 h group and 1.47 (0.70, 2.67)/mm2 in 72 h group. The microemboli burden in sham group was significantly different with groups after SAH at every observation time (P = 0.000, for all). Among the groups after SAH, the differences of microemboli burden were all significant at different observation times (P = 0.000, for all). Conclusion The extensive distribution of microemboli after SAH in both hemispheres may contribute to delayed cerebral ischemia. The time course of microemboli burden presents the dynamic course of microembolic formation and dissolution.

Key words: Subarachnoid hemorrhage, Cerebral arteries, Thrombosis, Disease models, animal

摘要： 目的   探讨蛛网膜下隙出血后迟发性脑缺血的发生机制，以期寻求新的治疗方法，提高蛛网膜下隙出血后脑缺血防治水平。方法   采用经颈动脉尼龙线颅内动脉刺破法建立小鼠蛛网膜下隙出血模型，通过大体标本和组织切片证实为蛛网膜下隙出血。免疫组织化学荧光染色法确认脑内微栓子形成，计数不同处理组动物平均微栓子数目（微栓子负载）。结果   微栓子呈簇状，散在分布于两侧大脑半球，无侧别差异。微栓子数目，假出血组0.00（0.00，0.05）个/mm2，蛛网膜下隙出血24 h 组0.29（0.11，0.46）个/mm2、48 h 组2.30（1.24，3.87）个/mm2、72 h 组1.47（0.70，2.67）个/mm2，假出血组与蛛网膜下隙出血组不同观察时间点（组）比较，微栓子数目差异有统计学意义（均P = 0.000）；蛛网膜下隙出血组不同观察时间点（组）之间，微栓子计数差异亦有统计学意义（均P = 0.000）。结论   蛛网膜下隙出血后脑血管内形成的、广泛分布的大量微栓子可能参与了迟发性脑缺血的发生机制，微栓子负载时程呈现血栓形成与溶解的动态变化过程。

关键词: 蛛网膜下腔出血, 脑动脉, 血栓形成, 疾病模型, 动物