We investigated in fetal sheep during late gestation the effects of acute
hypoxemia on fetal plasma
S100beta protein concentrations and how these relate to fetal redistribution of blood flow and
acid-base status. Under
general anesthesia, five Welsh Mountain sheep fetuses were instrumented with
vascular catheters, and transit-time flow transducers were implanted around a femoral artery and an umbilical artery. At least 5 d after surgery, fetuses were subjected to 1 h of normoxia, 0.5 h of
hypoxemia, and 1 h of recovery.
Hypoxemia induced significant falls in fetal pH(a), arterial
oxygen pressure,
acid-base excess, and [HCO(3)(-)], without alteration to arterial partial pressure of
carbon dioxide. An increase in arterial blood pressure, a fall in heart rate, an increase in femoral vascular resistance, and a decrease in umbilical vascular resistance occurred in all fetuses. During
hypoxemia, plasma S100beta increased significantly and remained elevated until the end of the protocol. Within individual fetuses, plasma S100beta correlated with femoral vascular resistance and pH. In contrast, no relationship was found between S100beta and umbilical vascular resistance. This study reports for the first time that a controlled period of fetal
hypoxemia with associated acidemia leads to persistent elevations in plasma S100beta concentrations that strongly correlate with hemodynamic changes that are known to occur during fetal blood flow redistribution. These findings open up a new role for changes in fetal S100beta concentrations as a possible early marker of
fetal hypoxia with associated acidemia in perinatal medicine.