Abstract 1728
Pulmonary: Control of Breathing Poster Symposium, Tuesday, 5/4
We have found previously that the infusion of a placental extract inhibits spontaneous fetal breathing in sheep during low voltage ECoG, suggesting that a placental factor may be responsible for the inhibition of fetal breathing. To determine whether known respiratory inhibitors such as PGE2, adenosine, or opioids present in the placental extract were responsible for this inhibition, we studied 6 chronically instrumented fetal sheep at 135±5 days of gestation. The infusion of a 1-10 kD placental extract inhibited breathing in 80% of the experiments (16/20) compared to 10% with the Krebs solution (1/10; p=0.0001). Sham infusions inhibited breathing in 11% of the experiments (1/9; p=NS compared to control). The concentration of PGE2 in the placental extracts was 2.0±0.8 ng/ml. This concentration of PGE2 was unlikely responsible for the inhibition of breathing observed with the placental extract since administration of PGE2 infusates at a higher concentration (10 ng/ml) inhibited breathing in only 6% of the experiments (1/16; p=NS compared to control). The concentration of adenosine in the placental extract was 36±1 ng/ml. The inhibition of breathing observed with placental extracts pretreated with adenosine deaminase (72% of the experiments; 13/18) was significantly different that control (p=0.004). Pretreatment of the fetus with naloxone had no effect in the inhibition of breathing observed with the placental extract (80% vs 89% of the experiments before and after treatment with naloxone; 8/10 vs 9/10; p=NS). These findings suggest that the inhibition of breathing observed with the placental extract is not related to PGE2, adenosine, or opioids. We speculate that a peptide produced by the placenta, not yet identified, with a molecular weight between 1-10 kD, inhibits fetal breathing.(Supported by the Children's Hospital Foundation)
