Abstract
Intimai hyperplasia is a major complication of vascular surgical procedures.1–5 In addition, intimai hyperplasia contributes significantly to the development of atherosclerosis.6 Hyperplasia is a result of platelet/leukocyte/injured vessel wall interactions, followed by the release of vasoactive, chemotactic and mitogenic substances which promote smooth muscle cells migration and proliferation.6, 7 Fatty acid metabolites synthesized by vascular wall and blood cells are thought to modulate, in part, the onset of intimai hyperplasia and atherosclerosis. For example, 13-hydroxyoctadecadienoic acid (13-HODE), derived from linoleic acid via the lipoxygenase pathway, has been shown to inhibit platelet adhesion to the subendothelial layer.8, 9 Since platelet adhesion to the vessel wall is a prerequisite to the secretion of platelet-derived smooth muscle cell, and linoleic acid is metabolized into 13-HODE the vessel wall, we determined whether a linoleic acid-rich diet, given before injury, was associated with decreased intimal hyperplasia following vessel wall balloon catheter injury in normo- and hypercholesterolemic rabbits.
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