Background Recently, endothelial dysfunction as a result of fetal cardiac bypass has been reported. Here, the effect of fetal cardiac bypass on the endothelial function of the umbilical artery was investigated by a tension study. Methods Fourteen fetal lambs were divided into a control group (n = 7) and a pump group (n = 7). In the pump group, cardiac bypass was maintained for 30 minutes using a low-volume priming circuit with a centrifugal pump. Hemodynamic measurements and blood gas analyses were performed before, during, and 30 and 60 minutes after cardiac bypass. The umbilical artery was harvested 60 minutes after cessation of cardiac bypass. Endothelium-dependent relaxation (bradykinin, calcium ionophore A23187) and endothelium-independent relaxation (sodium nitroprusside) were measured after smooth muscle contraction by 60 mmol/L potassium or serotonin and compared between the two groups. Results The umbilical artery flow and aortic pressure of the fetus were significantly decreased at 30 and 60 minutes after cardiac bypass. Hypoxia and hypercapnia were recognized during and after cardiac bypass. Metabolic acidosis progressed during and after cardiac bypass. Endothelium-dependent relaxation was impaired in the pump group compared with the control group (bradykinin: 43.6% ± 6.4% in the control group, 18.9% ± 2.5% in the pump group, p < 0.01; A23187: 37.8% ± 4.6% in the control group, 19.6% ± 3.9% in the pump group, p < 0.01). Meanwhile, endothelium-independent relaxation was preserved in both groups. Conclusions Fetal cardiac bypass caused endothelial dysfunction of the umbilical artery and hemodynamic deterioration as a result of metabolic acidosis. Prevention of endothelial damage and metabolic acidosis could be the main target for successful fetal cardiac surgery. © 2004 by The Society of Thoracic Surgeons.
Oishi, Y., Masuda, M., Yasutsune, T., Boku, N., Tokunaga, S., Morita, S., & Yasui, H. (2004). Impaired endothelial function of the umbilical artery after fetal cardiac bypass. Annals of Thoracic Surgery, 78(6), 1999–2003. https://doi.org/10.1016/j.athoracsur.2004.05.057