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THE PHYSIOLOGY OF PRE‐ECLAMPSIA
Author(s) -
Brown Mark A.
Publication year - 1995
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1995.tb01937.x
Subject(s) - medicine , endocrinology , eclampsia , prostacyclin , placenta , vasoconstriction , angiotensin ii , trophoblast , blood pressure , fetus , pregnancy , biology , genetics
SUMMARY 1. Pre‐eclampsia is a multisystem disorder of human pregnancy with a genetic predisposition. It occurs more commonly in first pregnancies and primarily affects maternal renal, cerebral, hepatic and clotting functions while elevating blood pressure. The foetus is affected through placental insufficiency arising from abnormal ‘placentation’, that is, failure of adequate trophoblast invasion of maternal vasculature, and possibly from abnormal autacoid production. 2. Pre‐eclampsia is caused by the placenta; delivery of the placenta is the only known cure. Its manifestations are considered secondary to organ hypoperfusion which arises as a result of vasoconstriction, intravascular coagulation and reduced maternal blood volume. 3. Current hypotheses propose that pre‐eclampsia is due to widespread maternal endothelial cell damage, perhaps secondary to a cytotoxic factor released by the placenta. This hypothesis has gained wide acceptance, but scientific evidence is lacking. 4. Defining the abnormal balance of vasoactive factors in pre‐eclampsia has proved a difficult task. There is enhanced pressor reactivity to infused angiotensin 11 (AII) despite reduced plasma concentrations of AII, renin and aldosterone. Prostacylclin production appears reduced, and the balance of thromboxane/prostacyclin favours vasoconstriction and platelet aggregation. There is no convincing evidence for enhanced endothelin or reduced nitric oxide production. Plasma concentrations of atrial natriuretic peptide are paradoxically elevated in the face of plasma volume contraction. An intriguing observation, which remains unexplained, is why some vascular beds are affected predominantly in one patient (eg. hepatic ischaemia) while another has a similar degree of hypertension but involvement of a different organ system (eg. renal insufficiency yet normal liver function). 5. Volume homeostasis is disturbed with redistribution of intravascular volume to the interstitial fluid space due to increased capillary permeability and in some cases reduced plasma oncotic pressure. This redistribution is not always clinically apparent as peripheral oedema. Whether this change in volume is compensated for by venoconstriction and maintenance of adequate cardiac output is undetermined. 6. Improved understanding of the pathophysiology of pre‐eclampsia is necessary to allow better clinical management of this serious disorder.