Irina Y Kuzmina1, Galina I Hubina-Vakulik, Graham J Burton. 1. Department of Obstetrics and Gynecology and Pathological Anatomy, Kharkhov State Medical University, St. Vesnina, 7-A, ap.13, Kharkov 61023, Ukraine. kuzmina@is.kh.ua
Abstract
OBJECTIVE: To investigate the structural basis of abnormal Doppler waveforms in the utero-placental circulations in cases of chronic fetal hypoxia. STUDY DESIGN: Morphometric analysis was performed on placental samples from 58 pregnancies with abnormal Doppler waveforms in the uterine, placental and umbilical circulations at 32-34 weeks, and 10 pregnancies with normal waveforms. RESULTS: The volume of placental villi reduced from 350.5 cm3 in controls to 286.4 cm3 (P<0.05) in the severest cases. The volume of the fetal capillaries reduced from 59.7 cm3 to 20.5 cm3 (P<0.05). These reductions were associated with increased placental infarction. The myometrial segments of the spiral arteries were severely constricted, demonstrating failure of physiological conversion secondary to deficient trophoblast invasion. CONCLUSION: The placental vascular bed is greatly reduced in cases of chronic fetal hypoxia. We propose impaired placental perfusion causes oxidative stress and regression of the fetal vasculature, leading to fetal growth retardation and distress.
OBJECTIVE: To investigate the structural basis of abnormal Doppler waveforms in the utero-placental circulations in cases of chronic fetal hypoxia. STUDY DESIGN: Morphometric analysis was performed on placental samples from 58 pregnancies with abnormal Doppler waveforms in the uterine, placental and umbilical circulations at 32-34 weeks, and 10 pregnancies with normal waveforms. RESULTS: The volume of placental villi reduced from 350.5 cm3 in controls to 286.4 cm3 (P<0.05) in the severest cases. The volume of the fetal capillaries reduced from 59.7 cm3 to 20.5 cm3 (P<0.05). These reductions were associated with increased placental infarction. The myometrial segments of the spiral arteries were severely constricted, demonstrating failure of physiological conversion secondary to deficient trophoblast invasion. CONCLUSION: The placental vascular bed is greatly reduced in cases of chronic fetal hypoxia. We propose impaired placental perfusion causes oxidative stress and regression of the fetal vasculature, leading to fetal growth retardation and distress.
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