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本文报道40例脑血栓患者,经口服硝吡苯啶药物治疗,有效率为87.5％,显效率为72.5％,其作用机制与硝苯吡啶能部分抑制缺血后细胞外钙离子进入细胞内,减少缺血性脑损伤有关。在用药前后采用两种诱导剂做了血小板聚集功能动态观察,治疗前血小板聚集性明显高于正常人(P<0.01)。提示:脑血栓患者血小板聚集性增高是形成血栓的关键。治疗后血小板聚集功能明显低于治疗前(P<0.01),说明硝苯吡啶具有降低血小板聚集功能,可能是钙离子拮抗剂抑制钙离子促发血小板聚集作用所致。
This article reports 40 cases of cerebral thrombosis patients treated with oral nifedipine, the effective rate was 87.5%, the effective rate was 72.5%, its mechanism of action and nifedipine can partially inhibit the extracellular extracellular calcium ions into the cells, Reduce ischemic brain damage related. Before and after treatment with two kinds of inducers to do the dynamic observation of platelet aggregation, platelet aggregation before treatment was significantly higher than normal (P <0.01). Tip: Increased platelet aggregation in patients with cerebral thrombosis is the key to thrombosis. Platelet aggregation after treatment was significantly lower than before treatment (P <0.01), indicating that nifedipine has a reduced platelet aggregation function, may be calcium ion antagonist inhibition of calcium-induced platelet aggregation caused by.