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Objective: This study describes a 24-hour assay of autonomic nervous system activity in human fetuses with the use of a power spectral analysis of heartbeat intervals., Study Design: The study included 6 normal fetuses and 11 growth-restricted fetuses, 3 of which were hypoxemic. Fetal heartbeats were continuously recorded for 24 hours, and a power spectral analysis was performed on the beat interval data. A low frequency domain of beat intervals was identified (0.025-0.125 cycles/beat) and evaluated at regular intervals over the 24-hour period. The cosinor method was used to detect rhythmic fluctuations in the resulting low frequency areas. The same procedures were also performed with the mothers of the fetuses., Results: We observed 2 diurnal rhythms of heartbeat activity (1 with a 12-hour period and another with a 24-hour period) in the normal and growth-restricted fetuses without hypoxemia. In contrast, these rhythms were not observed in the hypoxemic fetuses. In the mothers, only the 24-hour rhythm was observed., Conclusion: The 12-hour cycle of autonomic nervous activity is present in normal fetuses.

Objective: The appearance of the sinusoidal heart rate pattern found on fetal cardiotocograms has not been fully explained, either physiologically or clinically. In this study we performed power spectral analysis on the sinusoidal heart rate pattern obtained by administration of arginine vasopressin and atropine sulfate to investigate its frequency components in fetal lambs with long-term instrument implantation., Study Design: Eleven tests were performed in 4 fetal lambs at 120 to 130 days' gestation. An artificial sinusoidal heart rate pattern was obtained by administration of atropine sulfate and arginine vasopressin in 9 tests. An autoregression model was used to compare the spectral patterns before and during the sinusoidal heart rate pattern., Results: Marked decreases in low-frequency (0.025-0.125 cycles/beat) and high-frequency (0.2-0.5 cycles/beat) areas were observed in the presence of the sinusoidal heart rate pattern. However, there were no significant changes in the very-low-frequency area (0.01-0.025 cycles/beat), which corresponds to the frequency of the sinusoidal heart rate pattern., Conclusion: The sinusoidal heart rate pattern may represent a very low-frequency component inherent in fetal heart rate variability that appears when low- and high-frequency components are reduced as a result of strongly suppressed autonomic nervous activity.

Objective: Our purpose was to test the hypothesis that chronic placental insufficiency and intrauterine growth restriction in fetal sheep causes a decrease in the number of fetal heart rate accelerations and fetal heart rate variability., Study Design: Chronically catheterized fetal sheep were embolized (n = 6) daily with 15 to 50 microns latex microspheres for 21 days between 0.74 and 0.88 of gestation into the abdominal aorta, until fetal arterial oxygen content was decreased by 40% to 50% of the preembolization value. Control animals (n = 6) received saline solution only. Signals from chest electrodes were analyzed on-line with the Sonicaid System 8000 in 2-hour epochs every 6 hours starting at 8 AM over the first 48 hours of hypoxemia and for 2 hours between 8 and 10 AM every other day from day 3 to day 21 of hypoxemia. Umbilical artery Doppler-derived resistance index and fetal plasma catecholamine concentrations were also measured., Results: Embolized fetuses had asymmetric intrauterine growth restriction and became chronically hypoxemic (p < 0.001) with a progressive increase in the umbilical artery resistance index (p < 0.001). During the first 48 hours of hypoxemia the number of accelerations and decelerations and both short- and long-term fetal heart rate variability increased initially, followed by a return to control levels by 20 hours after the onset of embolization. After 21 days of hypoxemia the number of accelerations was significantly reduced by 30% compared with controls (p < 0.05). Both short- and long-term fetal heart rate variability in control fetuses gradually increased with advancing gestational age (p < 0.001 and p < 0.01, respectively), whereas in embolized fetuses the fetal heart rate variability remained unchanged and was 20% lower than that of controls on day 21 (both p < 0.01)., Conclusion: Intrauterine growth restriction and long-term hypoxemia in fetal sheep are associated with a decrease in short- and long-term fetal heart rate variability, possibly because of a delay in the normal maturational changes of the autonomic control of fetal heart rate.

Objective: Our goal was to determine the effect of chronic and acute umbilical-placental embolization on placental hemodynamic and fetal heart rate patterns in relation to fetal oxygenation in the near-term ovine fetus., Study Design: Daily fetal placental embolization was performed during 10 days in 9 sheep fetuses until fetal arterial oxygen content decreased by approximately 30%. Nine control fetuses received saline solution. Mean and pulsatile umbilical blood flow, perfusion pressure, placental vascular resistance, fundamental impedance, pressure pulsatility index, and umbilical artery resistance index corrected to a fetal heart rate of 160 beats/min were measured. On day 10 both groups were acutely embolized until fetal arterial pH decreased to approximately 7.00. Fetal heart rate was measured with the Sonicaid System 8000 (Oxford Sonicaid, Oxford, United Kingdom)., Results: Chronic fetal placental embolization was associated with a progressive reduction in umbilical blood flow (p < 0.00001) and fetal arterial oxygen content (p < 0.001) whereas fetal heart rate patterns remained unaltered. A chronic increase in umbilical artery resistance index corrected to a fetal heart rate of 160 beats/min could be entirely explained only if the changes in umbilical artery pressure pulsatility index and the fundamental impedance were taken into account, in addition to the changes observed in placental vascular resistance. During acute embolization leading to a 50% reduction in umbilical blood flow (p < 0.0002) and a three times increase in placental vascular resistance (p < 0.0001), the most consistent change in fetal heart rate patterns related to progressive metabolic acidosis was an 84% decrease in absolute acceleration frequency (p < 0.0001) whereas short-term fetal heart rate variability remained unaltered., Conclusion: Changes in umbilical artery resistance index induced by chronic umbilical-placental embolization resulting in fetal hypoxemia occurred before any changes in fetal heart rate patterns were detectable. A decrease in the absolute acceleration frequency was the only component of fetal heart rate patterns related to progressive metabolic acidosis in the near-term ovine fetus.

Objective: The purpose of this study was to examine the effect of chronic fetal placental embolization on fetal plasma prostaglandin E2 concentrations., Study Design: Fourteen pregnant sheep were studied (seven embolized and seven controls) for 10 days between 0.84 and 0.91 of gestation. Daily injections of nonradioactive microspheres were made to decrease fetal arterial oxygen content by 30% to 35% of preembolization values., Results: In response to repeated embolization, fetal plasma prostaglandin E2 concentrations increased significantly on day 1, declined to near control levels on days 2 to 6, but were significantly elevated again after day 7. Maternal prostaglandin E2 levels remained unchanged throughout the study. Fetal plasma prostaglandin E2 levels increased significantly with decreasing fetal oxygenation when fetal arterial oxygen content was < 2.0 mmol/L., Conclusion: We conclude that there is increased production of prostaglandin E2 by the placenta during progressive fetal hypoxemia induced by fetal placental embolization. We speculate that the progressive increase in prostaglandin E2 may be an important hormonal adaptive mechanism to maintain fetal homeostasis during the development of placental insufficiency.