EFFECTS OF INCREASED RESISTANCE TO UMBILICAL BLOOD-FLOW ON FETAL HEMODYNAMIC-CHANGES INDUCED BY MATERNAL OXYGEN ADMINISTRATION - A DOPPLER VELOCIMETRIC STUDY ON THE SHEEP

A fetal lamb model was used to investigate whether the effects of mate rnal O2 administration on fetal blood gases and hemodynamics were modi fied when the fetoplacental circulation was compromised by stepwise co mpression of both umbilical veins. At basal State, O2 administration i ncreased O2 saturation (SaO2) and the pulsatility index (PI) of the ca rotid artery Doppler wave form (p < 0.01). The first compression decre ased left ventricular output (-21 +/- 16%, mean +/- 1 SD, p < 0.01) an d umbilical mean velocity (-22 +/- 28%, p < 0.01) but did not modify c arotid pH, SaO2, or the PI in any of the arteries studied. At this lev el of compression, O2 administration increased carotid SaO2 (P < 0.01) but did not affect carotid PI. After a second compression, left ventr icular output and umbilical mean velocity were even more reduced [-39 +/- 21% (p < 0.01) and -53 +/- 23% (p < 0.01), respectively]. With thi s compression, carotid pH, SaO2, and PI decreased, whereas umbilical a nd descending aorta PI increased. O2 administration at this level of c ompression increased carotid Sao2 (p < 0.01) but did not modify caroti d PI. Throughout the three stages of the experiment, O2 administration did not affect umbilical PI, descending aorta PI, or umbilical mean v elocity. A good linear relationship (r = O.77, p < 0.001) was demonstr ated between left ventricular 02 delivery and carotid PI. Thus, at bas al state, O2 administration induced velocity changes compatible with a n increase in cerebral vascular resistance. With an increase in umbili cal vein resistance, this response was no longer demonstrated, even at a level of vein compression not significantly affecting carotid, umbi lical, or descending aorta PI. These results support future use of fet al Doppler velocimetry during maternal hyperoxygenation as a method to evaluate fetal 02 reserve and fetoplacental hemodynamic function.