Experimental study on intracerebral microembolic distribution in subarachnoid hemorrhage model

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.

DOI：10.3969/j.issn.1672-6731.2010.03.017