Abstract

The placenta can be severely infarcted and yet return well oxygenated blood in spite of the potential shunt paths produced. Optimisation of oxygen transport by some form of local flow matching has been suggested, either via a direct action of hypoxia on subchorial vessels, or indirectly by syncytiotrophoblastic metabolic products. Using casts of cotyledonal vessels and software modelling, a mechanism of hypoxic fetoplacental vasoconstriction could be demonstrated. A simple previously described passive placental model was extended to include hypoxic sensitive arteries and dependence of syncytio-trophoblastic metabolism on intervillus (maternal) blood oxygen content. Such a mechanism of placental flow matching could maintain fetal pO2 by reducing flow through inadequately oxygenated cotyledons, therefore optimising pO2 at the expense of flow. A further modification stabilising fetal water transfer was required to avoid changes in intervillus oxygen delivery producing changes in fetal water content via placental capillary pressure alterations. Intervillus/villus flow matching is likely in the human placenta and this study suggests probable biologically plausible mechanisms for such a phenomenon.

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