PHENYL-ISOPROPYL ADENOSINE (PIA) CAUSES ALTERATION IN FETAL ELECTROCORTICOGRAM (ECoG) PATTERN AND CASSATION OF FETAL BREATHING MOVEMENTS (FBM) IN THE FETAL SHEEP

Abstract

In studying the control of ECoG and FBM, we equipped 4 fetal lambs with intratracheal, amniotic, vascular catheters and ECoG electrodes. 2 of these were equipped with EKG electrodes. After 48 hours recovery, at 0.9 gestation, continuous recordings of tracheal and amniotic pressures, ECoG and EKG were begun. During 1000 minute control periods, low voltage high frequency (LVHF) ECoG predominated 61.5% of the total time. FBM occurred 35.6% of the total time and only during the LVHF ECoG. PIA, a known agonist for both Al and A2 receptors, 0.125mg (0.050mg/kg estimated fetal weight) was given intravenously to each fetus during established LVHF ECoG and FBM. LVHF ECoG converted in 45 ±30 seconds (mean ±S.E.M.) to high voltage low frequency (HVLF) ECoG which persisted for 12 ±2 minutes. These were followed by an intermediate ECoG pattern, neither LVHF or HVLF, that persisted for 125 ±15 minutes. FBM ceased within 2 ±1 minutes and did not recur over the subsequent 143 ±22 minutes. A rebound increase in FBM (51.0% of the total time) occurred over the subsequent 500 minutes (control 35.6%) without a significant increase in the LVHF ECoG. No significant changes in blood gases were observed. By inspection, EKG tracings in 2 fetal sheep showed a several second decrease in fetal heart rate (175 ± 7 BPM to 95 ± 7 BPM) and a several minute loss of beat-to-beat variability. Similar subtle changes have been seen with doses between 0.001 and 0.01mg/kg. We conclude that fetal ECoG, FBM, HR and beat-to-beat variability are influenced by adenosine and its receptors.