Abstract
A rise in central adenosine concentrations most likely triggers the inhibitory effects of acute hypoxia on fetal breathing movements. During prolonged O2 deficiency, the incidence of fetal breathing increases ove time, an adaptation which may involve down-regulation of adenosine receptors. Therefore, isovolemic anemia was induced in chronically catheterized fetal sheep to determine the effects of acute O2 deprivation on the affinity of brainstem A1 adenosine receptors. Compared to control values, the mean hemoglobin concentration in 4 fetuses was lowered by 54% (to 3.7 ± 0.4 g/dl) for 1 h and in 3 fetuses by 58% (to 3.8 ± 0.6 g/dl) for 4 h. Mean preductal arterial pH during anemia was significantly reduced to values as low as 7.123 ± 0.090, but mean paO2 and paCO2 were not significantly affected. The average incidence of fetal breathing movements was decreased by 80% during the first hour and by 50% during the fourth hour of anemia. In 3 fetuses with normal hemoglobin levels, about 32 ± 6.0% of the A1 adenosine receptors in the brainstem were in the high affinity state. After 1 h of anemia, the percentage of high affinity receptors in the pons (but not medulla or midbrain) had significantly increased to 47 ± 2.9%, but after 4 h of anemia all 3 brainstem regions had A1 receptor affinity within the range of control values. It is concluded that acute anemia induces a short-lived up-regulation of pontine A1 adenosine receptors, but anemia does not alter A1 receptor coupling in the midbrain where A1 receptors related to breathing inhibition may be located.