Objective To investigate the hypothesis that, should there be an increase in deported syncytiotrophoblast microvillous membrane fragments in pre-eclampsia, it may cause maternal vascular endothelial dysfunction.Design Syncytiotrophoblast microvillous membrane (STBM) vesicles, prepared from normal term placentae, were perfused through small subcutaneous arteries isolated from fat biopsies obtained at caesarean section. Endothelial function of these arteries was studied by determining acetylcholineinduced relaxation after preconstriction with noradrenaline. As controls, physiological buffer or red blood cell membranes in physiological buffer were used and endothelial function similarly estimated. Transmission electron microscopy was performed on arteries after perfusion.Sample STBM vesicles, isolated from the placentae of three healthy women undergoing elective caesarean section for reasons unrelated to pre-eclampsia, were suspended in physiological buffer. Subcutaneous fat arteries were obtained from a separate group of 13 normotensive pregnant women, also undergoing elective caesarean section at term.Results Perfusion with red blood cell membranes or physiological buffer had no significant effect on the concentration dependent relaxation in arteries preconstricted with noradrenaline. However, after 2 h perfusion with STBM vesicles, arteries showed a significant reduction in relaxation to acetylcholine, indicative of altered endothelial function. Transmission electron microscopy of arteries perfused with STBM vesicles confirmed endothelial disruption.Conclusions STBM vesicle perfusion specifically altered the relaxation response of preconstricted maternal subcutaneous fat arteries to acetylcholine, suggesting an alteration in endothelial dependent relaxation. Deported microvilli may therefore be capable of producing endothelial cell damage and endothelial dysfimction observed in the maternal syndrome of pre-eclampsia.

Objective To measure nitric oxide synthase activity in tissues from the placenta, placental bed and umbilical cord at delivery in normal and complicated pregnancies. Design A prospective blinded study. Setting The obstetric departments of three London teaching hospitals. Subjects Samples of whole placenta, dissected stem villous arteries, umbilical cord vessels and the placental bed of the uterus were collected at delivery and assayed for nitric oxide synthase activity. Samples of placenta were taken from ten normotensive, six pre‐eclamptic and eight growth retarded pregnancies, and stem villous arteries from a further seven normotensive pregnancies. Results There was minimal placental bed nitric oxide synthase activity in each group. Placental villous homogenates from pregnancies complicated by pre‐eclampsia and fetal growth retardation had significantly lower activities of nitric oxide synthase than those from normotensive women with appropriately grown babies. There were no significant differences in calcium dependent or calcium independent nitric oxide synthase activities in the umbilical vein and artery in the normal or in the pre‐eclamptic groups. However, there was significantly more calcium dependent than calcium independent nitric oxide synthase in the umbilical veins in all groups. Conclusions Local nitric oxide production in the placental bed of the uterus is unlikely to contribute substantially to the low resting vascular tone in the uteroplacental circulation. However, a relative deficiency of placental nitric oxide in pregnancies complicated by fetal growth retardation and pre‐eclampsia may contribute to the development of the high impedance fetoplacental circulation found in these conditions.

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A population of 2029 pregnant women (929 primiparas; 1100 multiparas) has been used to examine aspects of the calculation of obstetric risk scores from the presence of individual risk factors. The findings have been related to fetal outcome in these pregnancies and the following conclusions were reached: (1) the use of Bayes theorem for the calculation of a risk score is superior to the simple addition of weighted risk factors; (2) the diagnostic efficiency of a risk score is somewhat reduced when the data base used for calculation of the score is derived from a population different from that of the current pregnancy; (3) there is almost total overlap of risk scores in women with satisfactory and unsatisfactory fetal outcome. It is concluded that risk scores can be used to identify a small group of women at particularly high risk; in the remainder of the population scores are unhelpful except perhaps to indicate the women who do not require an intensive program of antenatal care.