Plasma From Patients With HELLP Syndrome Increases Blood–Brain Barrier Permeability. (March 2015)

• Record Type: Journal Article
• Authors: Wallace, Kedra; Tremble, Sarah M.; Owens, Michelle Y.; Morris, Rachael; Cipolla, Marilyn J.
• Is Part Of: Reproductive sciences. Volume 22:Number 3(2015:Mar.)
• Page Start: 278
• Page End: 284
• Publication Date: 2015-03
• Subjects: HELLP syndrome -- blood–brain barrier permeability -- myogenic response; Reproductive health -- Periodicals; Reproduction -- Periodicals; 612.6
• DOI: 10.1177/1933719114549844
• Languages: English
• ISSNs: 1933-7191

Abstract

Circulating inflammatory factors and endothelial dysfunction have been proposed to contribute to the pathophysiology of hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome. To date, the occurrence of neurological complications in these women has been reported, but few studies have examined whether impairment in blood–brain barrier (BBB) permeability or cerebrovascular reactivity is present in women having HELLP syndrome. We hypothesized that plasma from women with HELLP syndrome causes increased BBB permeability and cerebrovascular dysfunction. Posterior cerebral arteries from female nonpregnant rats were perfused with 20% serum from women with normal pregnancies (n = 5) or women with HELLP syndrome (n = 5), and BBB permeability and vascular reactivity were compared. Plasma from women with HELLP syndrome increased BBB permeability while not changing myogenic tone and reactivity to pressure. Addition of the nitric oxide (NO) synthase inhibitor N ω -nitro-l -arginine methyl ester caused constriction of arteries that was not different with the different plasmas nor was dilation to the NO donor sodium nitroprusside different between the 2 groups. However, dilation to the small- and intermediate-conductance, calcium-activated potassium channel activator NS309 was decreased in vessels exposed to HELLP plasma. Thus, increased BBB permeability in response to HELLP plasma was associated with selective endothelial dysfunction.