Objective To investigate the relationship between changes of vascular elasticity and spontaneous rupture of hepatocellular carcinoma (HCC). Methods We examined the semiquantitatively expression of related angiogenesis factors including von Willebrand factor, elastin and neutrophil elastase in 30 specimens of HCC with spontaneous rupture by immunohistochemistry compared with 30 specimens of HCC without rupture. Results The results showed that there was a significant decrease of von Willebrand factor, overproliferation of elastin and abnormal distribution of neutrophil elastase around the small artery in ruptured HCC. These changes exacerbated weakness of the blood vessels and destroyed function of coagulation. The blood vessels split easily when the vascular load increased from hypertension or minor mechanical trauma. Conclusion The spontaneous rupture of HCC may be related to the vascular dysfunction.
Objective To review the strategies on repairing elastic fibers in aorta. Methods Literature concerningelastic fiber as well as its repairment was consulted and summarized from three aspects: enhancement of the expressions ofits components, improvement of the condition of its assembly, and reduction of the destructive effects. Results Elastinis concerned as the main protein to be enhanced with three different methods including gene transfection, stimulationwith ectogenesis factors, and induction of phenotype transition of smooth muscle cell. Fibul in and lysyl oxidases show theabil ity to improve the assembly of the elastic fiber, while the related mechanisms are not clear. Matrix metalloproteinasesare regarded as the main destructive factors, and researches focus on reducing their expression as well as their destructiveeffects. Conclusion To assure a high-qual ity repair of elastic fibers in aorta, their components should be sufficientlyexpressed and effectively assemblyed, and the destructive effects caused by dangerous factors should also be reduced.
