中文摘要：

目的：从血小板角度分析血瘀形成的机制。方法：20只大鼠,按体质量随机分成空白组和寒凝血瘀组,寒凝血瘀组按照冰水浴加注射肾上腺素的方法连续造模15 d。禁食不禁水12 h后,第16天以乌拉坦1 mg/kg麻醉,固定,颈总动脉取血,测与血小板相关的各项指标。结果：与空白组比较,寒凝血瘀组血浆黏度、PDW极显著升高（P〈0.01）;PLT极显著降低（P〈0.01）;TXB2、β-TG、FN显著增高（P〈0.05）;6-keto-PGF1α、CAMP、CGMP均有降低趋势,但是无显著影响;VWF、PF4、MPV有升高趋势,无统计学意义。结论：寒凝血瘀形成机制可能是通过影响TXB2,FN,β-TG来促进血小板黏附、聚集作用,进而导致血瘀的形成。

英文摘要：

Objective： To investigate the biological difference in platelet rats with blood stasis by cold stagnation. Methods：Twenty Wistar rats were randomly assigned to a blank control group and a cold stagnation and blood stasis group. The blood stasis group was in accordance with the method of ice water bath and injection of epinephrine building for 15 days in a row. Platelet indexes were determined after 15 days. Results： Compared with the blank control group,plasma viscosity and PDW in model group were increased significantly. PLT was decreased significantly. The contents of TXB2,FN and β-TG were increased significantly（ P〈0. 05）. There was no significant difference in the contents of 6-keto-PGF1α,VWF,MPV,etc. Conclusion： Haemorrheological nature formation mechanism of blood stasis may be by influencing the TXB2,FN,β-TG to promote platelet adhesion and aggregation,leading to the formation of blood stasis.