During normal pregnancy, important physiological adaptations occur in the mother which assure an adequate blood supply to the fetus. Vascular resistance, mean arterial pressure, and sensitivity to endogenous constrictors are reduced, in addition to increased cardiac output, heart rate, and blood volume. Alteration of these haemodynamic adaptations to pregnancy is associated with conditions critical to fetal well-being such as pre-eclampsia (PE) and intrauterine-growth retardation (IUGR), characterized by endothelial dysfunction. The human placenta is a multifunctional organ providing oxygen, water homeostasis, nutrition and endocrine messages for the fetus until delivery. Impaired placental perfusion is associated with reduced transfer of oxygen and nutrients from the mother to the fetus. Consequently, fetal growth and oxygenation are reduced resulting in intrauterine growth retardation (IUGR) and fetal hypoxemic hypoxia. In humans, increased placental resistance may be the result of different factors: reduction in the number of placental terminal capillaries and small muscular arteries in the tertiary stem villi, increased vasoconstriction at villous level because of local release of vasoactive substances, e.g. thromboxane or endothelin, or decrease of vasorelaxant agents. These alterations are triggered by ischemia of the intervillous space due to reduced utero-placental perfusion.
Alan : Sağlık Bilimleri
Dergi Türü : Uluslararası
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