Human aortocoronary grafts and nitric oxide release: Relationship to pulsatile pressure

Background. Short and long-term failure of saphenous Vein grafts continues to be a significant problem for cardiac surgeons. The purpose of this study was to elucidate the early adaptive changes of human artery and vein condu its with respect to nitric oxide (NO) production under various pressure and pulsatile distention conditions. Methods. Real-time amperometric NO determinations were made in an in vitro model using human saphenous vein segments (n = 12) and internal thoracic ar tery segments (n = 8) between 70 and 170 mm Hg, under static conditions rec orded with a pressure transducer. Exposing the tissue to morphine (10(-6) M ) also stimulated NO release. Under conditions in which the conduits were e xposed to the respective pressures for 1 hour, they were then examined for their granulocyte-adhering potential using computer-assisted imaging techni ques. Results. A pressure-dependent decrease of NO release was found after 32 min utes of pulsatile pressure (170 mm Hg) in artery and vein, the latter of wh ich appeared to be affected more negatively (p < 0.05; because many more ob servation points differed significantly after 32 minutes compared to 110 mm Hg values). In vessels maintained for 1 hour at these different pressures and then exposed to morphine (1 mu M), stimulated NO release significantly diminished in the veins (artery 37.4 nM NO versus vein 18.1 nM NO; p < 0.05 ). Increased pressures also correlated with an increase in granulocyte adhe sion to veins that could not be reduced following morphine exposure. Conclusions. Increased pressure and cyclic distention lead to loss of NO re lease and increased immunocyte adhesion, which are significantly more prono unced in saphenous vein than in internal thoracic artery, suggesting that i n the long term this may contribute to the failure of saphenous vein condui ts in coronary revascularization. (C) 2000 by The Society of Thoracic Surge ons.