AI Article Synopsis
- The study aims to investigate hemodynamic changes and the role of "blood stasis" in liver fibrosis in rat models.
- Rats with liver fibrosis were created using pig serum injections, and various blood parameters were measured to assess changes compared to control rats.
- Significant increases in blood viscosity and liver fibrosis markers were found in the model rats, indicating that "blood stasis" may contribute to the development of liver fibrosis and supporting potential treatment strategies focusing on improving blood circulation.
Article 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), procollagen 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.
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