The effect of induced maternal hyperthermia (1.5 degrees C rise over 60 min) on the uterine and umbilical circulations was examined in two groups of chronically instrumented pregnant sheep. Hyperventilation occurred in both groups. In the group in which the resultant respiratory alkalosis was untreated (N = 5), uterine blood flow decreased to 53 +/- 3% (mean +/- SE; P less than 0.01) of control at maximal maternal temperature. Umbilical blood flow also decreased 30 +/- 6% (P less than 0.01) below control levels. In the other group, normocapnia was maintained (N = 4). Uterine blood flow decreased in this group to 75% +/- 2% (P less than 0.01) of control levels, but umbilical blood flow did not significantly change. There was no significant change in maternal or fetal mean arterial pressure during hyperthermia in either group. Thus, maternal hyperthermia per se results in a significant decrease in uterine blood flow primarily through an effect on uterine vascular resistance, but without a concomitant change in umbilical blood flow.
Baseline mean AVP levels were identical in ewes and fetuses (0.7 f 0.1 pU/rnl). After 30 min of hypoxia, plasma AVP levels remained unchanged in the ewes (0.9 2 0.1), but increased dramatically in the fetuses (47 f 21 pU/ml) (P < 0.001). There was a highly significant correlation between the duration of hypoxia and log fetal AVP concentrations (r = 0.85). The log fetal plasma AVP also was inversely correlated to the log fetal Po2 values (r = 0.83).Mean baseline fetal and maternal plasma OT levels were 2.6 2 0.5 pU/ml and 2.2 f 0.5 pU/ml, respectively. After 30 min of hypoxia fetal and maternal OT values were 2.9 f 0.8 pU/ml (not significant). Abbreviations AVP, arginine vasopressin OT, oxytocinAVP and OT contents of the fetal pituitary and hypothalamus increase during gestation (18, 21). Fetal plasma AVP and OT levels are low during the last third of gestation and although the placenta is impermeable to AVP and probably OT, basal maternal and fetal blood concentrations of AVP and OT are similar (7,12, 22, 23); however, it is clear that the ovine fetus is capable of responding to both osmotic and hypovolemic stimuli with AVP release early in the third trimester. After delivery, cord blood plasma AVP levels in newborn sheep and human infant are increased, more so after vaginal delivery than after Cesarian section delivery (I, 2, 3, 9, 10, 14, 15). This AVP elevation has been attributed to cerebral compression (6, 9) or stress and hypoxia (4,5,16).Several studies using bioassay as well as radioimmunoassay methods for measuring AVP have shown that hypoxia is a potent stimulus for fetal AVP release (1,17, 25). These studies often combined hypoxia with hypercarbia however, and none measured the OT response.In fact, little is known concerning OT responsiveness in the fetus. We and others have shown that cord blood plasma OT levels are elevated (2, 13), and there has been speculation that this elevation also may be due to hypoxia associated with delivery. The present study was undertaken to investigate the magnitude and timing of the AVP and OT responses to hypoxia, the latter as a single stimulus unassociated with hypercapnia and/or asphyxia. MATERIALS AND METHODSAnimal preparation. Ketamine was administered to four datebred ewes (Columbia-Suffolk), three with singleton fetuses and one with twin fetuses. The fetuses were 125-129 d gestational age. Hysterotomy was performed, the fetal leg was exteriorized, and a catheter was inserted into the fetal dorsal vein and artery and advanced to the inferior vena cava and dorsal aorta. The fetal leg was then replaced in the uterus, the fetal catheters were exteriorized to a pouch attached to the flank of the ewe, the uterine incision was sutured and maternal abdominal wall was closed. Femoral venous and arterial catheters were inserted into the ewe. Catheters were maintained patent with a dilute heparin solution (I U/4 ml blood).Chloramphenicol was given to the ewe (250 mg) and the fetus (25 mg), and instilled into amniotic fluid (250 mg) twice a day for five d postoperatively. ...
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