Coronary artery disease is the major cause of mortalilty in the West with coronary artery bypass surgery (CABG) being a means of restoring blood supply to ischaemic myocardium. The long saphenous vein is the most commonly used bypass conduit but its patency is inferior to the internal thoracic artery, the ‘gold standard’ graft. In conventional procedures the saphenous vein is harvested in such a manner that considerable vascular damage is inflicted. The structures mainly affected by this vascular trauma are the endothelium, autonomic nerves and vascular smooth muscle all containing cells with the potential to release nitric oxide (NO). While the majority of studies into the potential role of NO in vein graft performance have focussed on the involvement of endothelial nitric oxide synthase (eNOS) less information is available regarding the role of the inducible isoform of nitric oxide synthase (iNOS). While the effects of eNOS-derived NO are principally beneficial, iNOS is generally associated with pathological conditions. While potential pathophysiological roles of iNOS are discussed in this review we also outline many studies suggesting that this isoenzyme plays an important role in maintaing vein graft patency in patients undergoing CABG, particularly when the saphenous vein is harvested with minimal surgical trauma.