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.
Keywords: Human saphenous vein, bypass graft, iNOS, nitric oxide, coronary artery disease.
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