Exclusion of the placenta during fetal cardiac bypass augments systemic flow and provides important information about the mechanism of placental injury.

The in utero correction of congenital cardiac malformations requires the availability of fetal cardiac bypass. One difficulty with fetal cardiac bypass is that very high flow rates are necessary when the placenta is left in the bypass circuit; the placenta requires about 40% of fetal cardiac output, which results in a normal cardiac output of 400 ml/kg per minute. Previous attempts to perform fetal cardiac bypass failed to consistently achieve these high flow rates because of cannula size limitations. On the basis of previous work done in our laboratory with an isolated-placenta model, which demonstrated that at normothermia the placenta would tolerate at least 30 minutes of cessation of umbilical blood flow, we hypothesized that exclusion of the placenta from the fetal cardiac bypass circuit would reduce fetal cardiac output by one half and allow us to obtain better systemic perfusion without compromising placental function. Cardiac bypass was performed in 20 late-gestation fetal lambs. In 10 lambs, no drugs were given; 5 served as controls in which the placenta was perfused; in the last 5, the placenta was excluded by clamping the umbilical cord during bypass. The latter 10 lambs were treated with indomethacin, which is known to improve placental blood flow after fetal cardiac bypass. We measured blood gases and determined regional blood flow with radiolabeled microspheres to assess placental function after bypass. The 5 control fetuses experienced rapid hypercapnea and hypoxemia after bypass, in association with minimal placental blood flow; when the placenta was excluded, arterial carbon dioxide tension rose somewhat more slowly, and placental blood flow after bypass was significantly better. When indomethacin was given, arterial blood gases in both groups showed a mild increase in carbon dioxide tension and similar placental blood flows (about 30% of baseline) after bypass. Indomethacin is known to block the vasoconstrictive response of the placenta to fetal cardiac bypass, implicating the release of vasoactive cyclooxygenase products as the cause of the adverse effects. In this study, placental perfusion on bypass without indomethacin caused much more severe placental dysfunction than did bypass with the placenta excluded from the circuit. The use of indomethacin improved postbypass placental function in both groups, but this effect was much more dramatic in the placenta-perfused group.(ABSTRACT TRUNCATED AT 400 WORDS)