目的：研究组氨酸对脑血栓形成的影响及可能机制．方法：采用光化学诱导“脑—心卒中”模型并给组氨酸（ｉｖ５ｍｇ·ｋｇ－１）治疗．结果：脑血栓形成后４和２４ｈ全血血小板聚集的峰值为（５１±０５）Ω和（４３±０５）Ω．心肌线粒体体积（Ｖ）、体密度（Ｖｖ）、面密度（Ｎｍ）及外膜表面（Ｓｖ１）增加（８２±５５，０５９±０１６，０１１±００３和２２±００５，Ｐ＜００１），但数密度（Ｎｖ）、内膜比表面（δ２）和嵴膜比表面（δ３）减少（００７±００２，２８±０８和２４±０７，Ｐ＜００１），心肌病理学改变有别于缺血性坏死和缺血再灌所致的心脏损伤．组氨酸治疗后，全血血小板聚集降为（２９±１１）Ω（Ｐ＜００１），与内膜有关的体视学参数可逆改变．结论：组氨酸可抑制全血血小板聚集，并减轻由于脑缺血所致的心肌线粒体损伤． Objective: To investigate the effect of histidine on cerebral thrombosis and its possible mechanism. Methods: The model of “brain-stroke” was induced by photochemistry and treated with histidine (iv5mg · kg-1). Results: The peak values ​​of platelet aggregation at 4 and 24 h after thrombosis were (51 ± 05) Ω and (43 ± 05) Ω. Myocardial mitochondrial volume (V), body density (Vv), surface density (Nm) and outer membrane surface (Sv1) increased (8  2  5  5,0  59 ± 0  16,0  11 ± 0  03 And 22 ± 005, P <001), but the number density (Nv), specific surface area (δ2) and specific surface area of ​​crest membrane (δ3) decreased (007 ± 002, 2 8 ± 08 and 24 ± 07, P <001). The pathological changes of myocardium were different from those of ischemic necrosis and ischemia-reperfusion. After treatment with histidine, whole blood platelet aggregation was reduced to (29 ± 11) Ω (P <001), and the endomicroscopic parameters of stereology were reversibly changed. Conclusion: Histidine can inhibit whole blood platelet aggregation and mitigate myocardial mitochondrial damage due to cerebral ischemia.