Purpose of Review: Pre-eclampsia remains a leading worldwide
cause of maternal death and of perinatal morbidity.
There remains no definitive treatment except delivery of the
fetus.
Recent Findings: Recent insights into the cardiovascular changes
that are evident prior to, during, and persist after preeclampsia
have improved understanding of the underlying pathophysiology—disruption
of normal endothelial function and decreased
nitric oxide bioavailability. S-nitrosoglutathione
(GSNO) is an endogenous S-nitrosothiol that acts as a NO pool
and, by replenishing or preventing the breakdown of GSNO,
endothelial dysfunction can be ameliorated. GSNO reductase
inhibitors are a novel class of drug that can increase NO
bioavailability.
Summary: GSNO reductase inhibitors have demonstrated improvement
of endothelial dysfunction in animal models, and
in vivo human studies have shown them to be well tolerated.