W.A.W. Walters

The Effects of Chronic Maternal Hypotension During Pregnancy

Summary The relationship between chronic maternal hypotension and obstetric outcome was examined retrospectively in a group of 134 pregnant women and compared with a normotensive control group. The hypotensive women had significantly increased risks of delivery before the 38th week of gestation, lower birth‐weight of babies for gestational age, and postpartum complications. In addition, the rates of preterm delivery before 37 weeks gestation, birth‐weight less than 2,500 g and significant meconium‐staining of the amniotic fluid were higher in the hypotensive group, although these results did not reach statistical significance.

Large Meningioma Complicating Pregnancy

EDITORIAL COMMENT: This case report was accepted for publication because of the clinical lesson it delivers, namely that intracranial tumours, although rare in pregnancy, may as the authors state ‘produce a wide variety of symptoms that are difficult to distinguish from the more common symptoms of pregnancy, including nausea, vomiting and headache’. This case suggests that examination of the optic fundi is essential in patients with neurological symptoms even when/especially when there is a history of psychiatric illness.

The control of fetal vascular resistance in the human placenta

Summary The human placenta, perfused after delivery at term, has revealed useful information about the control of placental fetal vascular resistance. The placenta is not innervated, resistance in the fetal circulation being controlled by myogenic mechanisms interacting with effects of autacoids. The fetal vasculature in vitro responds readily to some vasoconstrictor autacoids, particularly thromboxane A 2 and endothelin-1. However the vasoconstrictor concentrations needed are well in excess of those normally present in umbilical blood. Efficient mechanisms exist in the fetal circulation to maintain its normal low resistance to blood flow. Amongst these is the fetal endothelium (and possibly the trophoblast), which in response to endogenous peptides such as corticotropin-releasing hormone, and shear forces caused by passage of blood releases the dilator autacoid nitric oxide. This interacts with prostacyclin to cause cell membrane stabilization and activation of intracellular vasodilator mechanisms in vascular smooth muscle. Hypoxia in the perfused healthy placenta causes fetal vascular sensitivity changes to autacoids similar to those found in placentae from some pre-eclamptic women. In particular fetal placental release of NO appears to be impaired by hypoxia. We also conclude that hypoxia in the fetal circulation which may occur during preeclampsia (with or without restricted fetal growth) and in pregnancies uncomplicated with pre-eclampsia when fetal growth restriction is present, could possibly contribute to placental fetal vasoconstriction and reduced blood flow.

The control of fetal vascular resistance in the human placenta: A review

Summary The human placenta, perfused after delivery at term, has revealed useful information about the control of placental fetal vascular resistance. The placenta is not innervated, resistance in the fetal circulation being controlled by myogenic mechanisms interacting with effects of autacoids. The fetal vasculature in vitro responds readily to some vasoconstrictor autacoids, particularly thromboxane A2 and endothelin-1. However the vasoconstrictor concentrations needed are well in excess of those normally present in umbilical blood. Efficient mechanisms exist in the fetal circulation to maintain its normal low resistance to blood flow. Amongst these is the fetal endothelium (and possibly the trophoblast), which in response to endogenous peptides such as corticotropin-releasing hormone, and shear forces caused by passage of blood releases the dilator autacoid nitric oxide. This interacts with prostacyclin to cause cell membrane stabilization and activation of intracellular vasodilator mechanisms in vascular smooth muscle. Hypoxia in the perfused healthy placenta causes fetal vascular sensitivity changes to autacoids similar to those found in placentae from some pre-eclamptic women. In particular fetal placental release of NO appears to be impaired by hypoxia. We also conclude that hypoxia in the fetal circulation which may occur during preeclampsia (with or without restricted fetal growth) and in pregnancies uncomplicated with pre-eclampsia when fetal growth restriction is present, could possibly contribute to placental fetal vasoconstriction and reduced blood flow.