Introduction: Increased plasma AVP contributes to the peripheral vasoconstrictor response to acute hypoxaemia in the fetus (Giussani et al. J.Physiol. 477, 81, 1994). We have shown that fetal pre-exposure to umbilical cord compression (UCC) sufficient to restrict fetal blood supply by 30%, markedly blunts the subsequent fetal vasoconstrictor response to hypoxaemia (Gardner et al. Circulation 106: 2278, 2002). This study determined whether this blunting is due to an effect on fetal plasma AVP concentration.
Methods: Under halothane anaesthesia, 15 fetal sheep were instrumented with an inflatable occluder around the umbilical cord, a Transonic flow probe around an umbilical artery and vascular catheters at 118 days of gestation. In 8 fetuses umbilical blood flow was reduced by 30% for 3 days beginning at 125 days by automated compression of the umbilical cord (UCC). The remaining fetuses acted as sham controls (n=7). At 130 pluminus 1 days, 2 days after recovery from cord compression, all fetuses were made hypoxic for 1h by maternal inhalational hypoxia. Maternal and fetal blood was taken at appropriate intervals during acute hypoxaemia for measurement of plasma AVP by validated RIA.
Results: Maternal basal plasma AVP was similar between groups and remained unchanged during hypoxaemia (2.5 plusminus 0.5 pg.ml-1). In contrast, a pronounced increase in plasma AVP occurred in control fetuses during hypoxaemia (4.8 plusminus 0.7 to 164±56 pg/ml). This increase was markedly blunted in UCC fetuses (6.1 plusminus 1.6 to 35 plusminus 9 pg/ml, P<0.05).
Conclusion: Suppression of the peripheral vasoconstrictor responses to hypoxaemia in previously cord-compressed fetuses may reflect, in part, blunting of the increase in plasma AVP concentration.
03 - 05 Nov 2003
Society for Endocrinology