Hill-West J L, Chowdhury S M, Slepian M J, Hubbell J A
Department of Biomedical Engineering, University of Texas, Austin 78712-1062.
Proc Natl Acad Sci U S A. 1994 Jun 21;91(13):5967-71. doi: 10.1073/pnas.91.13.5967.
Thin hydrogel barriers formed on the inner surface of injured arteries by interfacial photopolymerization dramatically reduced thrombosis and intimal thickening in rat and rabbit models of vascular injury. This polymerization technique allowed the synthesis of a thin hydrogel barrier that conformed to the vessel wall, directly blocking contact between blood and the damaged vessel. The illumination conditions could be varied to control the thickness of the barrier from 10 microns to > 50 microns. The hydrogel was designed to degrade by nonenzymatic hydrolysis. In rats in which the carotid artery had been severely injured by crushing, treatment with the hydrogel barrier completely eliminated thrombosis (P < 0.01) and preserved long-term patency (P < 0.01). Treatment in a rabbit model of balloon injury inhibited thrombosis (P < 0.02) and reduced long-term intimal thickening by approximately 80% (P < 0.003). These results suggest that blood-borne signals acting in the early phases of healing play an important role in stimulating thickening of the intima.
通过界面光聚合在受伤动脉内表面形成的薄水凝胶屏障，在大鼠和兔血管损伤模型中显著减少了血栓形成和内膜增厚。这种聚合技术能够合成一种贴合血管壁的薄水凝胶屏障，直接阻断血液与受损血管之间的接触。光照条件可以改变，以将屏障厚度控制在10微米至大于50微米之间。该水凝胶设计为通过非酶水解降解。在颈动脉因挤压而严重受伤的大鼠中，用水凝胶屏障治疗完全消除了血栓形成（P < 0.01）并保持了长期通畅（P < 0.01）。在兔球囊损伤模型中的治疗抑制了血栓形成（P < 0.02），并使长期内膜增厚减少了约80%（P < 0.003）。这些结果表明，在愈合早期起作用的血源性信号在刺激内膜增厚中起重要作用。
