The effect of uterine vascular insufficiency on fetal arterial pressure and heart rate in the near-term sheep.
Fetal hypoxia secondary to uterine vascular insufficiency was induced by injecting norepinephrine or PGE2 into the maternal circulation of near-term sheep. With these drugs the uterine blood flow fell to 41 and 40% of its control value, respectively. The fetal responses to the PGE2-induced uterine contraction were a bradycardia which was apparent within 10 seconds (P less than 0.05), and a hypertension which was also apparent within 10 seconds (P less than 0.03). After the norepinephrine-induced uterine vasoconstriction, there was no observable change in the fetal arterial pressure. The fetal heart rate started to fall after 30 to 60 seconds and started to return to the control value within 90 seconds. The fetal response to uterine vascular insufficiency induced by a contraction may not have been caused by hypoxia alone as these responses were more rapid in onset than the fetal responses observed subsequent to uterine vascular insufficiency produced by vasoconstriction.[1]References
- The effect of uterine vascular insufficiency on fetal arterial pressure and heart rate in the near-term sheep. Rankin, J.H., Phernetton, T.M. Obstetrics and gynecology. (1977) [Pubmed]
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