Link between abnormal placentation and endothelial dysfunction

The link between abnormal trophoblast invasion and endothelial cell dysfunction in the pathogenesis of pre-eclampsia is unclear. It is postulated that factor(s) elaborated by the hypoperfused placenta are disseminated via the circulation to various vascular beds resulting in endothelial dysfunction and neutrophil activation. A number of substances have been proposed, but the current focus is on the possible role of 'oxidative stress' and deported trophoblast elements.

'Oxidative stress'

Lipid peroxidation normally occurs at low levels in all cells and tissues under the regulation of a variety of antioxidant mechanisms. Placental production of lipid peroxide has been localized to the trophoblast cells. Serum lipid peroxidation products are elevated in normal pregnancy and further augmented in women with pre-eclampsia (Hubeleta/ 1996). Serum antioxidant activity is increased in normal pregnancy and reduced in pre-eclampsia, particularly in late gestation. Increased peroxidative activity may alter the structural and functional integrity of biological membranes and cause endothelial dysfunction.

Deported syncytiotrophoblast basement membrane

In pre-eclampsia, the microvilli of the syncytiotrophoblast are abnormally shaped, with focal areas of syncytiotrophoblast necrosis and loss. Syncytiotrophoblast microvillous membranes are shed into the maternal circulation in increased amounts. In vitro studies have demonstrated that syncytiotrophoblast basement membrane interferes with endothelial cell growth and may mediate endothelial dysfunction in pre-eclampsia.

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