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目的复制心血瘀阻证大鼠模型动态形成过程并进行方证验证。方法采用高脂饲养与冠状动脉左前降支结扎术结合的方法建立3阶段模型,即第一阶段“血瘀证前期”模型,第二阶段“亚血瘀证期”模型,第三阶段“心血瘀阻证期”模型,并设相应模型对照组及假手术组、阳性药物干预对照组、阴性药物干预对照组,每组8只。成模后采用阳性药物、阴性药物干预法验证动物模型,阳性药物干预组和阴性药物干预组大鼠分别在心血瘀阻证期造模后给予养心通脉片溶液3.25 g/(kg·d)和四逆散溶液3.00 g/(kg·d)灌胃,心血瘀阻证期组给予纯净水(1 ml/100 g)灌胃,共7天。观察各组大鼠中医表征积分,检测血液流变学、血脂指标。结果血瘀证前期组、亚血瘀证期组、心血瘀阻证期组中医表征积分均较本模型相应的对照组升高(P<0.05);心血瘀阻证期组、亚血瘀证期组血脂各指标均较本模型相应的对照组升高(P<0.05);血瘀证前期组、亚血瘀证期组与各自模型对照组比较血浆黏度水平升高(P<0.05)。血浆黏度和全血黏度中切比较,阳性药物干预组低于阴性药物干预组和心血瘀阻证期组(P<0.05)。结论通过3阶段造模法以及方证验证,初步建立了心血瘀阻证动态演变的实验动物模型。
Objective To replicate the dynamic process of rat model of heart stasis and verify the prescription. Methods The high-fat diet and left anterior descending coronary artery ligation combined with the establishment of three-phase model, the first phase of “blood stasis syndrome” model, the second phase of “blood stasis period” model, the first Three stages of “blood stasis syndrome period” model, and set the corresponding model control group and sham operation group, positive drug intervention control group, negative drug intervention control group, 8 in each group. After the model was established, the positive drug and the negative drug intervention were used to verify the animal model. The positive drug intervention group and the negative drug intervention group were given Yangxintongmai solution 3.25 g / (kg • d ) And Sini San solution (3.00 g / (kg · d)) were given intragastrically. Pure blood (1 ml / 100 g) was given intragastrically for a total of 7 days in the syndrome of stagnant blood stasis syndrome group. The scores of TCM symptoms in each group were observed, and the hemorheology and serum lipids were measured. Results The scores of TCM symptoms in the early stage of blood stasis syndrome, the blood stasis syndrome period and the period of syndrome of stagnant blood stasis syndrome were all higher than those in the corresponding control group (P <0.05). The blood stasis syndrome stage, Compared with the corresponding control group, the levels of serum lipids increased significantly in the model group (P <0.05). Compared with the model control group, plasma viscosity increased in the early stage of blood stasis syndrome and the control group of the same blood stasis syndrome group (P <0.05). Plasma viscosity and whole blood viscosity in the middle compared with the positive drug intervention group was lower than the negative drug intervention group and the blood stasis blocking group (P <0.05). Conclusion The experimental animal model of the dynamic evolution of blood stasis syndrome was established preliminarily through three stages modeling and verification.