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Hypothesis: inhibition of endothelium-derived relaxing factor by haemoglobin in the pathogenesis of pre-eclampsia
P M Sarrel1, D C Lindsay, P A Poole-Wilson
1Department of Cardiac Medicine, National Heart and Lung Institute, London, UK.
Although the aetiology of pre-eclampsia is unknown, haemodynamic studies suggest that many of the clinical findings may be explained by a generalised vasoconstrictive disorder and abnormal endothelial cell function. Vasoconstriction may be attributed to the increased concentrations of haemoglobin found in pre-eclampsia compared with normal pregnancy. Free haemoglobin may be derived from haemolysis and placental haemorrhage and, at concentrations known to be present in pre-eclampsia, vasodilatation mediated by endothelium-derived relaxing factor is inhibited. Infusion of oxyhaemoglobin into human coronary arteries inhibits acetylcholine-induced vasodilatation. We suggest that an increased free haemoglobin concentration is the cause of vasoconstriction in pre-eclampsia.
Although the aetiology of pre-eclampsia is unknown, haemodynamic studies suggest that many of the clinical findings may be explained by a generalised vasoconstrictive disorder and abnormal endothelial cell function. Vasoconstriction may be attributed to the increased concentrations of haemoglobin found in pre-eclampsia compared with normal pregnancy. Free haemoglobin may be derived from haemolysis and placental haemorrhage and, at concentrations known to be present in pre-eclampsia, vasodilatation mediated by endothelium-derived relaxing factor is inhibited. Infusion of oxyhaemoglobin into human coronary arteries inhibits acetylcholine-induced vasodilatation. We suggest that an increased free haemoglobin concentration is the cause of vasoconstriction in pre-eclampsia.