Rk. Silver et al., EVALUATION OF NITRIC-OXIDE AS A MEDIATOR OF SEVERE PREECLAMPSIA, American journal of obstetrics and gynecology, 175(4), 1996, pp. 1013-1017
OBJECTIVE: Our purpose was to determine whether a reduction in nitric
oxide synthesis occurs in women with severe preeclampsia as a conseque
nce of soluble serum factors. STUDY DESIGN: Circulating nitrate and ni
trite levels were compared between women who met standard clinical cri
teria for severe preeclampsia (n = 21) and maternal or gestational age
-matched, normotensive, primagravid control subjects (n = 21). End-pro
ducts of nitric oxide synthesis were measured from venous blood sample
s using nitrate reduction and chemiluminescence. To detect in vitro su
ppression of nitric oxide synthesis, human umbilical vein endothelial
cell monolayers were grown to confluence and exposed to culture media
containing 20% severe preeclamptic or control sera. Nitrate and nitrit
e production were compared in duplicate monolayers for each experiment
al condition, expressed as means +/- SEM in picomoles per 10(6) cells.
Data were compared by Student's t or Mann-Whitney U tests, when appro
priate, along with Spearman correlations for comparisons of laboratory
and clinical data. RESULTS: Circulating nitrate and nitrite levels we
re similar in normotensive and preeclamptic cohorts (976 +/- 88 vs 100
9 +/- 41 pmol/ml, respectively; p = 0.22), and no correlations between
blood pressure and nitric oxide metabolite levels were observed for t
he control or severely preeclamptic subsets. Similar patterns of in vi
tro endothelial nitrite production were observed after 1-, 12-, and 24
-hour incubations with 20% control or preeclamptic sera. CONCLUSIONS:
Circulating nitrate and nitrite levels are not reduced in patients wit
h severe preeclampsia compared with normotensive controls, and sera fr
om these women do not suppress endothelial cell nitric oxide synthesis
in vitro.