Pre-eclampsia (PE), fetal growth restriction (FGR), pre-term labour and fetal death are common complications of pregnancy often associated with abnormal maternal inflammation. Though the precise causes of these complications remain obscure, altered maternal blood flow to the placenta is an underlying hallmark, especially with respect to the pathogenesis of PE, FGR and fetal demise. Furthermore, deficient trophoblast-mediated spiral artery remodelling is often cited as the primary cause of impaired utero-placental perfusion. Considerably less attention has been directed towards investigating other factors, including maternal vasoconstriction or hemostatic alterations, as contributors to poor utero-placental perfusion. This review provides a rationale for investigating the role of abnormal maternal inflammation in the pathophysiology of pregnancy complications including PE, FGR and fetal demise. In particular, the association between aberrant maternal inflammation and inadequate utero-placental perfusion is considered in the context of inflammation-associated alterations in maternal hemostasis and vasoconstriction. Finally, the role of aberrant maternal inflammation as a cause of local oxidative/nitrosative stress is examined and the possibility of targeting deficient nitric oxide signalling as a therapeutic intervention for the treatment of inflammation-associated pregnancy complications is discussed.
Keywords: Fetal death; Fetal growth restriction; Hemostasis; Inflammation; Nitric oxide; Nitroglycerin; Oxidative stress; Placenta; Pre-eclampsia; Pre-term labour; Spiral artery remodelling; Tumour necrosis factor; Utero-placental perfusion; Vasoconstriction.
Copyright © 2015. Published by Elsevier Ltd.