THE EFFECTS OF 21 OR 30-PERCENT O2 PLUS UMBILICAL-CORD OCCLUSION ON FETAL BREATHING AND BEHAVIOR

We have shown previously that continuous fetal breathing can be induced by 100% O2 alone or combined with umbilical cord occlusion (Baier, Hasan, Cates, Hooper, Nowaczyk & Rigatto, 1990). To know whether it could also be induced by lower O2 concentrations plus cord occlusion, we studied 9 chronically instrumented fetal sheep (16 experiments) using our window model. After a baseline cycle [1 low voltage + 1 high voltage electrocortical activity (ECoG) epoch] the fetal lung was distended via an endotracheal tube to about 30 cm H2O. Inspired N2 (control) and 21 or 30% O2 were given for one cycle each. While on 21% or 30% O2 the umbilical cord was occluded (balloon cuff). In 10 out of 16 experiments breathing output (% maximum of integral EMG(di) X f) increased after cord occlusion from 80 +/- 48 (N2) to 2871 +/- 641 (SEM; P<0.01); in 7 of them breathing became continuous. Arterial PO2 increased from 14 +/- 1 (N2) to 33.5 +/- 5 Torr (occlusion; P<0.01). In the other 6 experiments breathing output decreased from 319 +/- 116 (N2) to 86 +/- 38 (occlusion; P<0.01) and arterial PO2 changed from 18 +/- 1 (N2) to 22 +/- 5 Torr (occlusion; P=0.4). Arterial PCO2 increased similarly after occlusion in both groups, those which did respond with increased breathing (to 46 +/- 2 Torr) and those which did not respond (to 48 +/- 3 Torr; P=0.6). The percent low voltage ECoG and the behavioral score increased after occlusion in the responder group only. The gestational age was 132 +/- 1 days in both groups. We suggest that: (i) continuous breathing and signs of arousal can be induced after cord occlusion in fetuses breathing an O2 mixture similar to that occurring at birth; and (ii) a modest increase in arterial PO2 (to about 30 torr) appears to be needed to counteract the inhibitory effect of hypoxia on fetal breathing.