Redistribution of power spectrum of heart rate variability during acute umbilical artery embolism and hypoxemia in late-gestation fetal sheep.

OBJECTS: Fetal heart rate variability (HRV) is subject to a number of factors, including fetal distress. The aim of this study was to investigate the power spectral distribution of fetal heart rate variability during acute hypoxemia following umbilical artery embolism and to test the hypothesis that the relative proportion of frequency domains in total power of HRV, reflects the changes in HRV during hypoxemia more closely than the absolute values. METHODS: Acute hypoxemia was induced in seven catheterized late-gestation fetal sheep by repeated injections of microspheres to cause umbilical artery embolism. The very-low, low-, middle- and high-frequency domains (0-0.025, 0.025-0.125, 0.125-0.20, and 0.20-0.50 cycles/beat, respectively) were determined by power spectral analysis. RESULTS: Umbilical artery embolism induced marked fetal hypoxemia, hypercapnia and acidosis, accompanied by an increase in heart rate and a decrease in arterial blood pressure. These changes were associated with the increase in power over the entire frequency range and in the relative power in the low-frequency range (P<0.01), and with decrease in the relative power in the high-frequency range (P<0.05). Correlations were found between the relative power in the low- and high-frequency ranges and PO2 and between the relative power in these ranges and mean arterial blood pressure (P<0.05), but not PCO2 or pH. CONCLUSIONS: The present study indicates that acute hypoxemia induced by umbilical artery embolism leads to the redistribution of power spectral density of fetal HRV and that the relative proportion of individual frequency domains may reflect the changes in HRV during acute hypoxemia more closely than the absolute power values.

[Effects of fetal anoxia and acidosis on superoxide dismutase].

OBJECTIVE: To analyze the effects of fetal anoxia, respiratory and metabolic acidosis on the activity of antioxidation in fetal distress. METHODS: Blood samples were taken from umbilical artery in 386 neonates for blood gas analysis and detection of the concentration of superoxide dismutase (SOD). Normal situation, anoxia, acidosis, respiratory acidosis, metabolic acidosis and mixed acidosis were diagnosed in all neonates according to the results of blood gas values, and the neonate asphyxia was diagnosed according to the Apgar scores (one minute). The effect of anoxia and acidosis to SOD were analyzed with multiple factor analysis of variation. RESULTS: (1) Among the all 386 cases, 317 were normal, 31 with anoxia, 17 with acidosis, and 21 with both anoxia and acidosis. Among the total cases of acidosis, 8 respiratory, 21 metabolic, and 9 mixed acidosis. (2) The plasma levels of SOD of umbilical artery blood in anoxia, acidosis, both anoxia and acidosis, and normal sitution were (118.5 +/- 7.1) mmol/L, (122.0 +/- 11.4) mmol/L, (140.0 +/- 7.0) mmol/L, and (98.5 +/- 2.6) mmol/L, respectively. The results of unvariate analysis of variance showed that anoxia: F = 4.999 (P < 0.05), acidosis: F = 7.025 (P < 0.01), and both anoxia and acidosis: F = 0.013 (P > 0.05). (3) The plasma levels of SOD with respiratory acidosis, metabolic acidosis and mixed acidosis were (127.3 +/- 18.4) mmol/L, (126.0 +/- 8.1) mmol/L, (150.0 +/- 10.4) mmol/L. The results of univariate analysis of variance showed that respiratory acidosis: F = 4.404 (P < 0.05), metabolic acidosis: F = 3.965 (P < 0.05), and mixed acidosis: F = 0.015 (P > 0.05). CONCLUSION: The superoxidation and antioxidation can be effected by factors like anoxia and acidosis, respiratory acidosis and metabolic acidosis. However, the mechanisms of these effects are different. There is additive, but not synergistic effects among them.