Background--The continuing incidence of intrapartum morbidity may be partly due to antenatal compromise, which influences the fetal defense to labor and delivery. We have shown that antenatal exposure of the ovine fetus to partial compression of the umbilical cord suppresses femoral vasoconstriction during subsequent acute hypoxemia through elevated nitric oxide (NO) activity. This study investigated whether elevated NO activity in cord-compressed fetuses enhanced the vasodilator response to hypoxemia in circulations in which blood flow is known to increase during acute hypoxemia, such as the umbilical vascular bed.

Methods and Results--Fifteen fetal sheep were chronically instrumented between 117 and 120 days of gestation with vascular catheters and an umbilical flow probe. In 8 of these fetuses, umbilical blood flow was reduced by 30% for 3 days between 125 and 128 days. The remaining 7 fetuses acted as sham-operated controls. Between 2 and 7 days after umbilical cord/sham compression, fetuses were exposed to 2 episodes of acute hypoxemia, on separate days, during infusion with either saline or treatment with a combination of N^G-nitro-L-arginine methyl ester and sodium nitroprusside. The data show that umbilical cord compression significantly enhances the umbilical hyperemia through NO-dependent mechanisms during a subsequent episode of acute hypoxemia.

Conclusions--Increased fetal NO activity after chronic cord compression has opposing effects in circulations that either constrict or dilate during subsequent acute hypoxemia. The data imply that antenatal compromise switches the fetal strategy to withstand episodes of subsequent acute hypoxemia of the type that may occur during labor and delivery from a reliance on vasoconstrictor mechanisms to those promoting NO-dependent vasodilation.