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动脉粥样硬化(AS)的形成与内皮损伤和脂质代谢异常有关,其病变特征为动脉内膜平滑肌细胞(smc)增生和脂质沉积。因此能引起内皮损伤、血脂升高及smc增生的因素均可促进AS的发生及发展。尽管AS的发病机制尚不十分清楚,但近年来对肝素及类肝素样物质的研究表明,肝素似乎与所有参与AS的生理过程有关。一、肝素对脂质代谢的影响肝素有明显降血脂用用。1943年Hahn发现肝素能消除狗的餐后实验性高脂血症,引起人们对肝素和AS关系的注意。但在体外用肝素
The formation of atherosclerosis (AS) is associated with endothelial damage and dyslipidemia, characterized by diseased arterial smooth muscle cell (smc) proliferation and lipid deposition. So can cause endothelial damage, elevated blood lipids and smc proliferation factors can promote the occurrence and development of AS. Although the pathogenesis of AS is not well understood, studies of heparin and heparinoid-like substances in recent years have shown that heparin appears to be involved in all physiological processes involved in AS. First, the impact of heparin on lipid metabolism Heparin has significant hypolipidemic use. In 1943, Hahn found that heparin can eliminate experimental postprandial hyperlipidemia in dogs, causing people to pay attention to the relationship between heparin and AS. But with heparin in vitro