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Clinical Science (2003) 104, (405–412) (Printed in Great Britain)

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Commentary on this paper

Evidence of impaired microvascular function in pre-eclampsia: a non-invasive study

N. ANIM-NYAME*, J. GAMBLE†, S.R. SOORANNA*, M.R. JOHNSON*, M.H. SULLIVAN‡ and P.J. STEER*

*Department of Maternal and Fetal Medicine, Imperial College School of Medicine at Chelsea and Westminster Hospital, 369 Fulham Road, London SW10 9NH, U.K., †School of Sport and Exercise Sciences, University of Birmingham, Birmingham B15 2TT, U.K., and ‡Institute of Reproductive and Developmental Biology, Imperial College School of Medicine, Hammersmith Hospital, Du Cane Road, London W12 0NN, U.K.

Key words: isovolumetric venous pressure, microcirculation, microvascular dysfunction, multisystem dysfunction, prediction of pre-eclampsia, pre-eclampsia.

Abbreviations: BMI, body mass index; ICAM-1, intercellular cell-adhesion molecule-1; K_f, filtration capacity; K_fU, K_f units; PV_i, isovolumetric venous pressure; V_a, vascular filling; VCAM-1, vascular cell-adhesion molecule-1; VCP, venous congestion pressure.

Correspondence: Dr N. Anim-Nyame (e-mail n.anim@ic.ac.uk).

The clinical presentation of pre-eclampsia suggests that microvascular dysfunction may play a role in the maternal manifestations of the disease. Isovolumetric venous pressure (PV_i) is an index of microvascular function, reflecting local plasma colloid osmotic (oncotic) pressure, and is abnormal in clinical conditions with microvascular dysfunction. We hypothesized that, in pre-eclampsia, post-capillary margination of neutrophils would increase post-capillary resistance, and therefore PV_i. A small cumulative step strain-gauge plethysmography protocol was used to compare PV_i in 18 women with pre-eclampsia, 16 normal pregnant women and 17 non-pregnant controls. Circulating levels of vascular cell-adhesion molecule-1 (VCAM-1), intercellular cell-adhesion molecule-1 (ICAM-1) and E-selectin, and neutrophil elastase, were measured to assess endothelial and neutrophil activation respectively. PV_i was significantly greater in the pre-eclampsia group, relative to the normal pregnant and non-pregnant controls (P<0.001, ANOVA, for both comparisons). PV_i was significantly lower during normal pregnancy compared with the non-pregnant controls (P = 0.001). Plasma levels of neutrophil elastase, VCAM-1, ICAM-1 and E-selectin (P = 0.001) were significantly greater in the pre-eclamptics than the controls. Significant positive correlations were observed between PV_i and neutrophil elastase (r = 0.71, P = 0.001), VCAM-1 (r = 0.52, P = 0.03), ICAM-1 (r = 0.67, P = 0.002), E-selectin (r = 0.69, P = 0.001), uric acid levels (r = 0.54, P = 0.02) and haematocrit (r = 0.64, P = 0.004) in pre-eclampsia. The relationship with the platelet count was negative (r =-0.65, P = 0.003). No significant correlations were observed between PV_i and maternal age, gestational age, total protein, albumin, diastolic blood pressures, age, body mass index and infant birth mass in the normal pregnant and non-pregnant controls. These data suggest that microvascular dysfunction occurs in pre-eclampsia, and that it is related to alterations in endothelial cell and neutrophil activation.

Received 14 November 2002; accepted 29 January 2003

The Biochemical Society and the Medical Research Society © 2003