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Objectives: The study analyzed the phase relationship between fetal heart rate and arterial blood pressure fluctuation during sinusoidal heart rate patterns in fetal lambs. Study Design: Thirty-two fetal lambs were placed on extracorporeal membrane oxygenation after cesarean delivery at ages ranging between 113 and 133 days' gestation. Sinusoidal heart rate patterns persisting for >10 minutes were analyzed. The relationships between the sinusoidal heart rate cycles and the arterial blood pressure cycles were quantitatively expressed in degrees by timing the zenith and the nadir of each and assigning a phase-angle index (with 0 [360] and 180 degrees being synchronized and reciprocal, respectively). Simultaneous blood samples were taken from the 4 different sites of the fetal circulation for blood gas and acid-base analysis when the sinusoidal heart rate pattern appeared. Regional cerebral blood flow was determined by means of the colored microsphere technique in 8 fetuses with sinusoidal patterns and 7 control fetuses. Results: Sinusoidal heart rate patterns were observed in 13 (40.6%) of the 32 fetal lambs. Two types of fetal heart rate and arterial blood pressure relationship could be recognized during sinusoidal pattern, the reciprocal type (n = 7) and the synchronized type (n = 9). A reciprocal type of sinusoidal pattern preceded a synchronized type pattern in 3 lambs that showed sinusoidal patterns at different stages of the experiment. The reciprocal type was associated with a higher baseline heart rate and amplitude of the sinusoidal heart rate pattern than was the synchronized type. The synchronized type was associated with a lower pH and base excess than was the reciprocal type. The cerebral blood flow in the medulla oblongata was significantly lower during the synchronized type pattern than during the reciprocal type pattern. Conclusion: There are 2 types of sinusoidal heart rate pattern. A synchronized type sinusoidal heart rate pattern may indicate more advanced fetal compromise than is associated with a reciprocal type pattern. (Am J Obstet Gynecol 1999;180:462-8.)

We previously showed that in asphyxiated fetal lambs the duration of hypotension correlated well with the severity of histologic damage to the brain, whereas the duration of bradycardia did not. This study compares fetal heart rate patterns with the degree of histologic damage to the brain.Twelve chronically instrumented near-term fetal lambs were subjected to asphyxia by umbilical cord occlusion until fetal arterial pH was6. 9 and base excess was-20 mEq/L. An additional 4 fetuses served as sham-asphyxia controls. Fetal heart rate (from electrocardiogram), arterial blood pressure, fetal breathing movements, and electrocorticogram were continuously monitored before, during, and for 72 hours after asphyxia. Fetal brain histologic features were categorized as mild (group 1, n = 5), moderate (group 2, n = 4), and severe (group 3, n = 3). Long-term fetal heart rate variability expressed as amplitude range was assessed visually every 5 minutes from 30 minutes before asphyxia until 2 hours of recovery and at 6, 12, 24, 48, and 72 hours of recovery.Long-term fetal heart rate variability amplitude decreased from 32 +/- 17 beats/min (mean +/- SEM) preocclusion to 4 +/- 13 beats/min at the end of occlusion (P.001) without significant differences among the 3 groups. During 10 to 45 minutes of recovery, the long-term variability of group 1 was significantly greater than that of groups 2 and 3. At 24 to 72 hours of recovery, the long-term variability of groups 1 and 2 was significantly higher than that of group 3, which was almost 0. The "checkmark" and sinusoidal fetal heart rate patterns were observed during the recovery period in groups 2 and 3.Decreased long-term fetal heart rate variability and the "checkmark" and sinusoidal fetal heart rate patterns were indicators of the severity of asphyxial histologic damage in the fetal brain.

Our purpose was to characterize the histologic changes in the asphyxiated fetal lamb brain and to correlate the severity of these changes with fetal physiologic parameters during and after asphyxia.Seventeen near-term fetuses were used for analysis: control group without manipulation (n = 4, 132 +/- 1.1 days of gestation at autopsy, mean +/- SEM), sham-asphyxia control group (n = 3, 132 +/- 1.3 days), and asphyxiated group, which successfully survived 72 hours after asphyxia (n = 10, 130 +/- 1.0 days). Asphyxia was produced by umbilical cord occlusion lasting for approximately 60 minutes until fetal arterial pH diminished to6.9 and base excess to-20 mEq/L. Fetal heart rate, blood pressure, and electrocorticographic activity were continuously monitored. The fetuses were killed 72 hours after asphyxia, and the brains were fixed in formalin and processed for histologic and immunocytochemical studies.Neuropathologic changes varied from case to case, ranging from almost total infarction of cortical and subcortical structures to extremely subtle and patchy white matter alterations characterized by slight vacuolization of the white matter or slight to moderate increases in cellularity confined to the junction of cerebral cortex and white matter. Even fetuses that showed full recovery of all physiologic parameters, including electrocorticographic activity, demonstrated subtle but distinct white matter lesions. The gray matter, including the hippocampal neurons, was generally spared in these cases. Electrocorticographic parameters, duration of hypotension during asphyxia, and delayed recovery of blood lactate concentrations correlated well with the histologic grading of brain damage.Asphyxia by partial umbilical cord occlusion in near-term fetal lambs produces variable neuropathologic changes. The mildest change is a white matter lesion characterized by vacuolization and loss of myelin or by increased cellularity in the damaged regions.

OBJECTIVES: The purpose of this study was to explain the role of oxidative stress in the pathogenesis of brain damage caused by intrauterine fetal asphyxia. STUDY DESIGN: Six chronically instrumented near-term fetal lambs were subjected to asphyxia by partial umbilical cord occlusion for approximately 60 minutes until fetal arterial pH diminished to less than 6.9 and base excess to less than –20 mEq. Another six fetuses surgically prepared but not occluded were used as control. Fetuses were killed after 72 hours and eight different brain regions (frontal and parietal gray matter, frontal and parietal white matter, basal ganglia, thalamus, hippocampus, and cerebellum) were dissected and assayed for thiobarbituric acid reactive substances, glutathione, and superoxide dismutase. RESULTS: Thiobarbituric acid reactive substance levels in asphyxiated animals were elevated in frontal and parietal white matter, basal ganglia, and thalamus compared with those in controls. The concentrations of superoxide dismutase in the asphyxiated group were also higher in frontal and parietal white matter, basal ganglia, and cerebellum compared with those in the control group. Between the two groups, however, glutathione concentrations did not differ significantly. CONCLUSION: These results suggest that oxidative stress may be a major contributing factor to the development of brain damage in intrauterine fetal asphyxia. (Am J Obstet Gynecol 1998;178:474-8.)