Pre-eclampsia is a pregnancy specific multi-system disorder associated with increased maternal and perinatal morbidity and mortality. In spite of intensive research for several decades into its pathophysiology, the aetiology remains unexplained. There is evidence that maternal tissue blood flow is reduced in pregnancies complicated by this disease, which precedes clinical onset, and persists after delivery. It is however unclear whether the reduced maternal tissue blood flow is associated with changes in tissue oxygenation and/or abnormal tissue oxygen homeostasis and whether this precedes or follows pre-eclampsia. This review examines the cause and effect relationship between hypoxia and pre-eclampsia and possible underlying mechanism(s) of impairment in oxygen regulation.
Keywords: Pre-eclampsia, endothelial dysfunction, hypoxia, implantation, oxygen sensing, oxygen tension, pregnancy, homeostasis, proteinuria, cardiovascular dis-eases, hypertension, maternal tissue hypoxia, endothe-lial dysfunction, oxygen homeostasis, Adenosine, prostagland-ins, nitric oxide, hypoxia-evoked vasodilatation, plasma adenosine levels, hypoxia inducible factor-1, oxygen-regulated gene expression, superoxide, insulin-like growth factors, vascular endothe-lial growth factor, endothelin-1, erythropoetin, transferrin, glucose trans-porter type 1, lactate dehydrogenase A, arteriovenous oxygen, Haemoglobin affinity, ischemic injury, hypovolemia, proinflammatory cytokines, haematocrit, cytotrophoblast, syncytiotrophoblast, trophoblast, uteroplacental circulation, myometrial spiral arteries, intrauterine fetal growth restriction, intervillous space, Doppler analysis, placental vascular remodelling, polygenic trait, glycogen phos-phorylase, lactate dehydrogenase, cytochrome C oxidase mRNA, ATP synthase
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