免疫性肝纤维化大鼠血液流变学研究

目的 观察免疫性肝纤维化大鼠血液流变学的变化,探讨肝纤维化"血瘀"的病机特点.方法 建立猪血清致大鼠肝纤维化模型,观察肝纤维化大鼠全血粘度150/s、30/s、5/s、1/s切变率及红细胞压积的变化,同时检测肝纤维化指标及血清转氨酶.结果 肝纤维化模型组的全血粘度150/s切变率、30/s切变率、5/s切变率、1/s切变率、红细胞压积、透明质酸酶、层粘连蛋白、Ⅲ型前胶原、Ⅳ型胶原、谷丙转氨酶、谷草转氨酶与正常对照组相比显著升高;且肝纤维化四项指标与全血粘度的各个切变率呈显著正相关.结论 肝纤维化大鼠血液流变学的变化特点一定程度上反应了肝纤维化"血瘀"的中医病机,为抗肝纤维化"活血化瘀"的治疗提供依据.

Abstract：

Objective To observe the changes in the hemodynamics of rats with immunological liver fibrosis and explore the pathogenesis of "blood stasis" in liver fibrosis. Methods Rat models of liver fibrosis were established by multiple intraperitoneal injections of pig serum. The hematocrit, blood viscosity at the shear rate of 150/s, 30/s, 5/s, and 1/s, serum markers for liver fibrosis, and serum transaminase levels were measured in the control and model rats. Results The hematocrit, blood viscosity at different shear rates, hyaluronic acid (HA), laminin (LN), procolagen type Ⅲ (PCⅢ), type Ⅳ collagen (CIV), glutamic-pyruvic transaminase (ALT) and glutamic-oxaloacetic transaminase (AST) increased significantly in the rats with experimental liver fibrosis appeared as compared with those in the control rats. Positive correlations were noted between blood viscosity at different shear rates and serum concentrations of the fibrosis markers (HA, LN, PCⅢ, and CIV) in the model rats. Conclusion The changes in the hemodynamics in rats with immunological liver fibrosis suggests the role of "blood stasis" in the pathogenesis of liver fibrosis and provide experimental evidence for therapies to "activate the blood circulation and dissipate blood stasis" for treatment of liver fibrosis.

Changes in the hemodynamics of rats with immunological liver fibrosis

Objective To observe the changes in the hemodynamics of rats with immunological liver fibrosis and explore the pathogenesis of "blood stasis" in liver fibrosis. Methods Rat models of liver fibrosis were established by multiple intraperitoneal injections of pig serum. The hematocrit, blood viscosity at the shear rate of 150/s, 30/s, 5/s, and 1/s, serum markers for liver fibrosis, and serum transaminase levels were measured in the control and model rats. Results The hematocrit, blood viscosity at different shear rates, hyaluronic acid (HA), laminin (LN), procolagen type Ⅲ (PCⅢ), type Ⅳ collagen (CIV), glutamic-pyruvic transaminase (ALT) and glutamic-oxaloacetic transaminase (AST) increased significantly in the rats with experimental liver fibrosis appeared as compared with those in the control rats. Positive correlations were noted between blood viscosity at different shear rates and serum concentrations of the fibrosis markers (HA, LN, PCⅢ, and CIV) in the model rats. Conclusion The changes in the hemodynamics in rats with immunological liver fibrosis suggests the role of "blood stasis" in the pathogenesis of liver fibrosis and provide experimental evidence for therapies to "activate the blood circulation and dissipate blood stasis" for treatment of liver fibrosis.