科研之友
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摘要
Introduction: Placental ischemia can be pre-placental (maternal), placental or post-placental (fetal), with corresponding changes in villous vasculature. Hydrops fetalis (HF) resulting from hemoglobin (Hb) Bart disease can serve as a model for intrauterine hypoxia, and placentas from such cases show a distinctive peripheral villous stromal myofibroblastic hypercellularity (PVSH). We hypothesized that Hb Bart disease, which results in profound fetal hypoxia, would lead to placental hypoxia on a post-placental basis. Methods: We assessed villous vasculature using computerized morphometry, comparing placentas in 14 Hb Bart HF cases to 18 non-Hb Bart HF cases. Morphometric parameters were matched as closely as possible to those reported in the literature for comparison purposes. Results: Villous vessels of Hb Bart HF showed significantly increased numbers of vessels (p = 0.001), longer vascular perimeter (p = 0.002), thickening of vascular endothelial layer (p = 0.038) and higher shape coefficient (p = 0.042) indicating a more branching pattern of vessels. In addition, placental villi of Hb Bart HF containing PVSH showed a longer vascular perimeter (p = 0.008) and narrower lumen (p = 0.002), with a higher shape coefficient (p = 0.03), in comparison to villi lacking PVSH. Discussion: Contrary to expectations, the overall pattern of vascular changes in Hb Bart HF suggested multifactorial hypoxia: pre-placental, on the basis of the marked placentomegaly, compromising blood flow from uterine distention; placental, from hydropic villi causing a generalized diminished intervillous space; and post-placental from the greatly reduced capacity of Hb Bart to extract oxygen from the intervillous space. Standardized vascular morphometry will facilitate comparison between different conditions, for a better understanding of placental hypoxia.
- 出版日期2016-8
