Chemoreceptor responsiveness in fetal sheep.

Fetal peripheral chemoreceptor responses to arterial O2 saturation and changes in PCO2 have not yet been quantitated. In 24 late-term chronically instrumented fetal sheep, we measured the heart rate response to acute hypoxemia induced by uterine arterial occlusion at various resting O2 saturations (25-86%) and at induced reductions and increases in baseline O2 saturation. As an index of fetal chemoreceptor responsiveness we calculated the fall in heart rate divided by the fall in arterial O2 saturation (delta HR/delta sat). delta HR/delta sat was inversely related to resting O2 saturation at levels less than 65%, but greater than 65% this relationship was no longer present. However, an induced increase in baseline O2 saturation from 66 +/- 12 to 76 +/- 10% decreased delta HR/delta sat from 2.6 +/- 1.6 to 1.8 +/- 1.0, indicating that when resting O2 saturation is greater than 65% there may be adaptation of peripheral chemoreceptors. Below 65%, an induced decrease in baseline O2 saturation increased delta HR/delta sat (to 3.8 +/- 1.8), suggesting a lack of adaptation to lower O2 saturations. Concomitant changes in PCO2, or differences in baseline PCO2, did not affect delta HR/delta sat during uterine arterial occlusion, which suggests that there is no interdependence between O2 and CO2 as a stimulus for the fetal peripheral chemoreceptor. However, acute hypercapnia (n = 24 in 8 fetal sheep) induced bradycardia. Furthermore, this bradycardia was related to the increase in fetal arterial PCO2. We conclude that the fetal peripheral chemoreceptor is sensitive to hypoxemia and hypercapnia and that the hypoxemia response is accentuated with decreases in initial O2 saturation.