Abstract
Restenosis after balloon angioplasty of vascu lar lesions in patients with atherothrombotic disease re mains an important complication of the procedure. At tempts to limit restenosis have been generally unsuccess ful. The endothelial cell normally produces several factors that limit the molecular and cellular events under lying the restenotic response. Chief among these is en dothelium-derived relaxing factor/nitric oxide. This sim ple molecule inhibits platelet activation, secretion, adhe sion, and aggregation; relaxes the underlying vascular smooth muscle cell; impairs leukocyte adhesion to the vessel wall; and limits vascular smooth muscle cell pro liferation. The mechanistic bases for these observations are presented in this overview, and experimental in vivo data that support the benefits of nitric oxide and nitric oxide donors in the prevention of restenosis are also re viewed.

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