Alteration of fetal oxygenation and responses to acute hypoxemia by increased myometrial contracture frequency produced by pulse administration of oxytocin to the pregnant ewe from 96 to 131 days' gestation.
OBJECTIVE
This study examined the effects of increased myometrial contracture frequency from 96 to 131 days' gestation on ovine fetal oxygen transport and physiologic response to acute hypoxemia.


METHODS
Ten pregnant ewes received either saline solution (control, n = 5) or long-term administration of oxytocin (600 microU. kg-1. min-1) in 5-minute pulses every 20 minutes to the maternal jugular vein beginning at 96 days' gestation (n = 5). Maternal tracheal tubes, fetal carotid artery and jugular vein catheters, and electrocorticographic and electromyographic electrodes were placed with the animals under halothane general anesthesia at 122 days' gestation. At 131 days' gestation fetal hypoxemia was induced for 1 hour. Maternal and fetal arterial blood gas samples were obtained at 60, 15, and 5 minutes before the start of hypoxemia and at 5, 10, 20, 30, 40, 60, and 120 minutes after the start of hypoxemia.


RESULTS
Baseline PO2 before hypoxemia was significantly lower and oxygen content was significantly higher in fetuses in the long-term oxytocin group than in control fetuses. At the end of hypoxemia the fetal pH, oxygen saturation, and oxygen content were significantly higher in the long-term oxytocin group than in the control group, although PO2 did not differ between groups. The fetal blood oxygen dissociation curve was shifted to the left in the long-term oxytocin group. During hypoxemia the absolute fetal blood pH was higher and the blood pH variation was lower in long-term oxytocin group than in the control group. Lower baseline and hypoxia-induced fetal plasma cortisol concentrations were observed in fetuses in the long-term oxytocin group than in fetuses of control ewes.


CONCLUSIONS
Increased contracture frequency during a period of 35 days shifts the fetal oxygen dissociation curve toward the left and alters fetal response to acute hypoxemia.
D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D005260:Female; D005312:Fetal Blood / Q000378:metabolism*; D005315:Fetal Diseases / Q000097:blood*; D005865:Gestational Age; D006854:Hydrocortisone / Q000097:blood; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000097:blood* / Q000209:etiology; D007700:Kinetics; D010100:Oxygen / Q000097:blood*; D010121:Oxytocin / Q000008:administration & dosage* / Q000494:pharmacology; D011247:Pregnancy; D012756:Sheep; D014590:Uterine Contraction / Q000187:drug effects*