INHIBITION OF THROMBOSIS AND INTIMAL THICKENING BY IN-SITU PHOTOPOLYMERIZATION OF THIN HYDROGEL BARRIERS
INHIBITION OF THROMBOSIS AND INTIMAL THICKENING BY IN-SITU PHOTOPOLYMERIZATION OF THIN HYDROGEL BARRIERS
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DOI：
10.1073/pnas.91.13.5967
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发表时间：
1994-06-21
影响因子：
11.1
通讯作者：
HUBBELL, JA
中科院分区：
文献类型：
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作者：
HILLWEST, JL;CHOWDHURY, SM;HUBBELL, JA
在大鼠和家兔血管损伤模型中，通过界面光聚合在损伤动脉内表面形成的薄水凝胶屏障可显著减少血栓形成和内膜增厚。这种聚合技术可以合成与血管壁一致的薄水凝胶屏障，直接阻断血液与受损血管之间的接触。在不同的光照条件下，可控制颈动脉屏障厚度在10 μ m ~ 50 μ m之间。水凝胶采用非酶解降解，在颈动脉挤压损伤大鼠中，水凝胶屏障完全消除血栓形成（P < 0.01），并保持长期通畅（P < 0.01）。在兔球囊损伤模型中，治疗可抑制血栓形成（P < 0.02），并使长期内膜增厚减少约80% （P < 0.003）。这些结果表明，在愈合的早期阶段，血源性信号在刺激内膜增厚中起重要作用。
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 mu m to >50 mu m 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 approximate to 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.