MECHANISMS OF ARTERIAL GRAFT HEALING

在过去的一年里，我们继续研究子宫内膜如何 聚四氟乙烯(PTFE)动脉移植物的增厚 在狒狒受伤的动脉中也是如此。我们一直在追寻这一假设 一氧化氮(NO)是平滑肌的主要负性调节因子 血管中的细胞(SMC)生长，因为高血流抑制 血管内膜增厚和诱导内皮型一氧化氮合酶 基因(EcNOS)。我们用药物阻断ecNOS原因的实验 血管收缩，但不会诱导SMC增殖，除非 某种程度的伤害。此外，我们还进行了实验 用抗血小板衍生生长因子受体的抗体(-( (PDGF-R-(-())定义PDGF在内膜增厚中的作用。PDGFR-( 阻滞剂抑制损伤或血管内皮损伤引起的血管内膜增厚 血液流动。我们还试图将我们的工作扩展到临床 申请。我们已经开发了一种外植体系统，并证明了 外植体中SMC的生长与损伤后SMC的生长非常相似 动脉。我们现在希望用外植体系统来定义 人大隐静脉外植体中人血管平滑肌细胞的特性。终极的 目标是在动物研究和结果之间提供联系 人类。

In the past year we continued our studies on how intimal thickening develops in polytetrafluoroethylene (PTFE) arterial grafts and in injured arteries in baboons. We have pursued the hypothesis that nitric oxide (NO) is a major negative regulator of smooth muscle cell (SMC) growth in blood vessels, because high blood flow suppresses intimal thickening and induces the endothelial nitric oxide synthase gene (ecNOS). Our experiments with agents to block ecNOS cause vasoconstriction but do not induce SMC proliferation unless there is some degree of injury. In addition, we have performed experiments with antibodies to platelet-derived growth factor receptor-(-( (PDGF-R-(-() to define a role for PDGF in intimal thickening. PDGFR-( blockade inhibits intimal thickening induced by injury or a switch in blood flow. We have also tried to extend our work to clinical application. We have developed an explant system and have shown that SMC growth in explants resembles very closely SMC growth in injured artery. We now hope to use the explant system to define the properties of human SMCs in saphenous vein explants. The ultimate goal is to provide a link between animal studies and outcome in humans.