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本文基于光化学反应机理，对大鼠缺血性卒中光化学模型进行研究，指出光化学反应诱导ＶＥＣ功能异常，从而加速了血小板聚集，导致血管栓塞。该模型制作简单，相对非侵害，有可能替代大脑动脉闭塞的缺血性卒中模型。
Based on the photochemical reaction mechanism, this paper studies the photochemical model of ischemic stroke in rats, and points out that the photochemical reaction induced the abnormal function of VEC, which accelerated the platelet aggregation and resulted in the embolization of blood vessel. The model is simple, relatively nonintrusive and has the potential to replace ischemic stroke models of cerebral artery occlusion.