The vasoregulatory role of endothelium derived nitric oxide during pulsatile cardiopulmonary bypass

The role of pulsatile flow as a physiologic stimulus for endothelium mediated vasoregulation is poorly understood. Furthermore, non pulsatile flow, which is associated with increased vascular resistance and end-organ failure, has been demonstrated to lead to a decrease in nitric oxide (NO) production in vitro. Anesthetized pigs (23.4 ± 0.3 kg) were placed on cardiopulmonary bypass using either non pulsatile or pulsatile perfusion for 60 min. In both groups, animals were maintained with a constant mean aortic flow (1.0-1.3 L/min). Serum samples obtained during bypass were assayed for the stable end-products of NO (nitrate [NO₃^-] and nitrite [NO₂^-]) by a method based on the Greiss reaction. Systemic vascular resistance was higher after 60 min in the non pulsatile (3712.5 ± 481.2 dyne sec cm^-5) vs the pulsatile group (2672.6 ± 427.0 dyne sec cm^-5), but not statistically significant (p > .05). However, NO production was decreased in the non pulsatile flow group (27 ± 6%) vs the pulsatile flow group (14 ± 5%) at a statistically significant level (p < .005). The results suggest that non pulsatile flow is associated with diminished endothelial shear stress and a reduction in endothelial nitric oxide production. This may contribute to the detrimental physiologic effects observed in prolonged non pulsatile flow states.