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Platelet thrombosis, intimal hyperplasia, and the progression of atherosclerosis are the most important factors determining the patency of vein grafts for arterial occlusive disease. Interactions between aggregating platelets and the vessel wall play an important role in all of these processes. The endothelium modulates the underlying vascular smooth muscle by releasing nitric oxide (NO), a potent vasodilator and anti-aggregating substance. This review focuses on vascular modulation by NO in vein grafts.

Mechanisms and prevention of intimal thickening of the autogenous vein grafts--possible involvement of nitric oxide--.