论文部分内容阅读
目的:探查中医肝郁脾虚证模型的血流变及相关调节因子的状态。方法:采用慢性束缚应激+过度疲劳+饮食失节法建立大鼠肝郁脾虚证模型,测定大鼠造模三周、自然恢复一周时的血流变和血浆TXB2、PGF1a。结果:与正常组相比,模型组大鼠造模三周150/s、38/s、10/s、5/s切变率下的全血粘度、还原粘度均显著升高(P<0.001),红细胞聚集指数显著降低(P<0.001),红细胞压积显著升高(P<0.01),红细胞变形指数无显著性差异(P>0.05);血浆TXB2显著升高(P<0.001),6-keto-PGF1a显著降低(P<0.05),TXB2/PGF1a显著升高(P<0.01);模型组大鼠第四周150/s、38/s、10/s、5/s切变率下的全血粘度、还原粘度仍显著升高(P<0.001或P<0.01);红细胞聚集指数显著降低(P<0.001);红细胞压积与变形指数无显著性差异(P>0.05);血浆TXB2和TXB2/PGF1a显著降低(P<0.05),6-keto-PGF1a显著升高(P<0.05)。结论:肝郁脾虚证大鼠存在血液高粘和血栓易形成状态,恢复期血液高粘同时伴有扩血管因素的加强。提示肝郁脾虚证有血流变的异常和血浆TXB2-PGI2的平衡失调,主要涉及到血小板和血浆因素的参与。
Objective: To investigate the state of blood rheology and related regulatory factors in TCM model of liver depression and spleen deficiency. Methods: The model of liver-qi stagnation and spleen-deficiency syndrome was established by chronic restraint stress, fatigue and eating disorders in rats. The blood rheology and plasma TXB2 and PGF1a were determined after three weeks and one week of natural recovery in rats. Results: Compared with the normal group, the whole blood viscosity and the reduced viscosity of the model group were significantly increased at 150 / s, 38 / s, 10 / s and 5 / s shear rate (P <0.001), hematocrit increased significantly (P <0.01), erythrocyte deformability index showed no significant difference (P> 0.05), plasma TXB2 increased significantly -keto-PGF1a and TXB2 / PGF1a significantly increased in the fourth week of the model group (P <0.05). In the fourth week of the model group, the shear rates of 150 / s, 38 / s, 10 / s and 5 / s (P <0.001 or P <0.01), the erythrocyte aggregation index (P <0.001), the hematocrit and deformation index were not significantly different (P> 0.05), and the plasma TXB2 And TXB2 / PGF1a (P <0.05), and 6-keto-PGF1a was significantly increased (P <0.05). Conclusion: The rats with stagnation of liver-qi and spleen deficiency have the status of hyperviscous blood clots and easy formation of blood clots, and the hyperviscosity of blood in convalescent phase is accompanied by the enhancement of vasodilators. Prompt liver depression and spleen deficiency abnormal blood flow and plasma TXB2-PGI2 balance disorders, mainly related to platelet and plasma factors involved.