Kibbe M, Billiar T, Tzeng E
University of Pittsburgh, Department of Surgery, PA 15261, USA.
Cardiovasc Res. 1999 Aug 15;43(3):650-7. doi: 10.1016/s0008-6363(99)00130-3.
The role nitric oxide (NO) plays in the cardiovascular system is complex and diverse. Even more controversial is the role that the inducible NO synthase enzyme (iNOS) serves in mediating different aspects of cardiovascular pathophysiology. Following arterial injury, NO has been shown to serve many vasoprotective roles, including inhibition of platelet aggregation and adherence to the site of injury, inhibition of leukocyte adherence, inhibition of vascular smooth muscle cell (VSMC) proliferation and migration, and stimulation of endothelial cell (EC) growth. These properties function together to preserve a normal vascular environment following injury. In this review, we discuss what is known about the involvement of iNOS in the vascular injury response. Additionally, we discuss the beneficial role of iNOS gene transfer to the vasculature in preventing the development of neointimal thickening. Lastly, the pathophysiology of transplant vasculopathy is discussed as well as the role of iNOS in this setting.
一氧化氮（NO）在心血管系统中所起的作用复杂多样。更具争议性的是诱导型一氧化氮合酶（iNOS）在介导心血管病理生理学不同方面所起的作用。动脉损伤后，NO已被证明具有多种血管保护作用，包括抑制血小板聚集和黏附于损伤部位、抑制白细胞黏附、抑制血管平滑肌细胞（VSMC）增殖和迁移以及刺激内皮细胞（EC）生长。这些特性共同作用以在损伤后维持正常的血管环境。在本综述中，我们讨论了关于iNOS参与血管损伤反应的已知情况。此外，我们还讨论了iNOS基因转移至血管在预防新生内膜增厚发展方面的有益作用。最后，讨论了移植血管病的病理生理学以及iNOS在这种情况下的作用。
