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本文采用静注虎红Ｂ（１０ｍｇ·ｋｇ－１体重）与滤过的特种光源（λ５６０ｎｍ，Δλ６０ｎｍ）反应诱导大鼠局部脑血栓形成，并以组织形态学（光镜及电子探针显微分析）、单线态氧测定（法拉第磁天秤法）及全血血小板聚集（阻抗法）为指标，观察光化学反应后上述指标的改变，以探讨血小板活化在脑缺血所致心功能异常发生中的作用。结果表明，光化学反应后，脑皮层顺磁性（磁化率）降低（Ｐ＜０．０５），全血血小板聚集增强（Ｐ＜０．０５），同时心功能明显抑制（Ｐ＜０．０５和０．０１）；５ｄ时，心功能的改变随血小板功能的下降而恢复至实验前水平。光化学反应后，神经元变性、坏死的病理学改变与脑实质和软脑膜血管内大量血小板聚集有关，即继发于脑血栓形成所致的脑缺血。
In this paper, local thrombosis was induced by intravenous injection of tiger red B (10 mg · kg-1 body weight) and filtered special light source (λ560nm, Δλ60nm), and histopathology (light microscope and electron probe microanalysis ), Singlet oxygen determination (Faraday magnetic scale) and whole blood platelet aggregation (impedance method) as indicators, to observe the changes of these indicators after photochemical reaction in order to investigate the role of platelet activation in the occurrence of cardiac dysfunction caused by cerebral ischemia . The results showed that paramagnetism (magnetic susceptibility) decreased (P <0.05), whole blood platelet aggregation increased (P <0.05), and cardiac function was significantly inhibited after photochemical reaction (P <0.05 and 0 .01). At 5 days, the changes of cardiac function recovered to pre-experimental level with the decrease of platelet function. After photochemical reaction, pathological changes of neuronal degeneration and necrosis are related to the accumulation of a large number of platelets in the parenchyma and pial vessels in the brain, which is secondary to cerebral ischemia caused by cerebral thrombosis.