Presented at the Neonatal Society 2001 Autumn Meeting.

Gardner DS, Fowden AL, Giussani DA

The Physiological Laboratory, University of Cambridge, UK

Umbilical cord compression and associated hypoxaemia are common intrauterine challenges that the fetus encounters during gestation. However, little is known about how the fetus adapts to prolonged compression of the umbilical cord or how adaptation to prolonged adverse intrauterine conditions influences the fetal capacity to mount an appropriate response to a subsequent acute ‘stress’ such as hypoxia, that may occur during labour and delivery. We have developed an automated system for controlled and reversible compression of the umbilical cord in the unanesthetised sheep fetus (1). Partial compression of the cord is maintained accurately for 3 days resulting in mild fetal asphyxia, an increase in mean arterial blood pressure and femoral vascular resistance and prevention of the ontogenic fall in fetal heart rate (1). During compression of the cord fetuses elicit a marked increase in hind limb glucose uptake and become lactacidaemic. After compression of the cord, umbilical flow and fetal blood gas status return to baseline levels. During subsequent acute hypoxaemia, the classic hypertension, bradycardia and peripheral vasoconstriction observed in controls is markedly blunted in cord-compressed fetuses. The mechanism for this blunting favours an up-regulation of vasodilatator activity such as nitric-oxide, rather than attenuation of vasoconstrictor function. In addition, cord-compressed fetuses show a re-setting of basal hypothalamo-pituitary-adrenal function during and after the period of the reduction in umbilical blood flow (2). These data show that fetal exposure to adverse conditions in utero alter the fetal defence mechanisms to subsequent acute stress. The data are important with regard to pre- and postnatal development of cardiovascular, endocrine and metabolic function and are especially relevant for the obstetric management of labour in pregnancies which have been complicated by antenatal adverse intrauterine conditions.

References
1. Gardner D. et al. J Physiol 2001; 535: 217-230
2. Gardner D. et al. Endocrinology 2001; 142: 589-598