RT Journal
A1 Chambers JC, Fusi L, Malik IS, Haskard DO, De Swiet M, Kooner JS
T1 ASsociation of maternal endothelial dysfunction with preeclampsia
JF JAMA
JO JAMA
YR 2001
FD March 28
VO 285
IS 12
SP 1607
OP 1612
DO 10.1001/jama.285.12.1607
UL http://dx.doi.org/10.1001/jama.285.12.1607
AB Context 
                  Preeclampsia is believed to result from release of placental factors
that damage maternal vascular endothelium. However, because most studies have
been conducted during pregnancy, it has not been possible to separate maternal
from placental mechanisms underlying endothelial dysfunction in preeclampsia.Objective 
                  To determine whether endothelial function is impaired in nonpregnant
women with previous preeclampsia and whether endothelial dysfunction is mediated
by oxidative stress.Design and Setting 
                  Case-control study conducted at 3 hospital maternity units in London,
England, between July 1997 and June 2000.Participants 
                  A total of 113 women with previous preeclampsia (n = 35 with recurrent
episodes; n = 78 with a single episode) and 48 women with previous uncomplicated
pregnancies, all of whom were at least 3 months (median, 3 years) postpartum.Main Outcome Measures 
                  Brachial artery flow-mediated (endothelium-dependent) and glyceryl trinitrate–induced
(endothelium-independent) dilatation were compared between previously preeclamptic
women and controls. To investigate oxidative stress, these measurements were
repeated after administration of ascorbic acid, 1 g intravenously, in 15 cases
and 15 controls.Results 
                  Mean (SD) flow-mediated dilatation was lower in women with previous
preeclampsia compared with controls (recurrent group, 0.9% [4.1%]; single-episode
group, 2.7% [3.5%]; and control group, 4.7% [4.3%]; P<.001).
In contrast, glyceryl trinitrate–induced dilatation was similar in the
3 groups (recurrent, 19.5% [5.9%]; single-episode, 21.0% [8.0%]; and control,
21.0% [8.3%]; P = .65). Impaired flow-mediated dilatation
in previously preeclamptic women was not accounted for by recognized vascular
risk factors. Ascorbic acid administration increased flow-mediated dilatation
in previously preeclamptic women (baseline, 2.6% [3.3%]; after administration,
5.6% [3.0%]; P = .001) but not in controls (baseline,
6.2% [3.3%]; after administration, 6.7% [5.0%]; P
= .72).Conclusions 
                  Our results indicate that endothelial function is impaired in women
with previous preeclampsia and is not explained by established maternal risk
factors but is reversed by antioxidant ascorbic acid administration.