@entity1827 and prostacyclin attenuate increases in hydraulic permeability caused by platelet-activating factor in XXXX .

@entity35 @entity5567 @entity295 @entity1827
We have previously documented that @entity1827 ( @entity1827 ) and prostacyclin (PGI2) decrease basal state hydraulic permeability (Lp). The aim of this study was to investigate the ability of @entity1827 and PGI2 to modulate transendothelial fluid flux during situations in which Lp was artificially elevated with platelet-activating factor ( @entity5567 ). We hypothesized that @entity1827 and PGI2 administration before @entity5567 exposure would prevent the increase in Lp secondary to @entity5567 . In addition, in a potentially more clinically relevant situation, we also hypothesized that @entity1827 and PGI2 administration after @entity5567 exposure would attenuate the increase in Lp secondary to @entity5567 . Microvascular Lp was measured in @entity35 mesenteric postcapillary venules. Exposure to 10 nM @entity5567 increased Lp 4-fold (P < 0.001). If the administration of 80 pM @entity1827 or 10 microM PGI2 was completed before @entity5567 exposure, no @entity5567 -associated increase in Lp was observed (P < 0.001). The administration of @entity1827 or PGI2 after @entity5567 exposure attenuated the peak increase in Lp caused by @entity5567 alone by 55% and 57%, respectively (P < 0.001). We conclude that @entity1827 and PGI2 administration before @entity5567 exposure prevents @entity5567 -induced elevations in Lp, and in a more clinically relevant situation, @entity1827 and PGI2 administered after @entity5567 exposure attenuate the @entity5567 -induced increase in Lp. @entity1827 and PGI2 receptors may provide important therapeutic targets for decreasing the microvascular fluid leak-associated morbidity resulting from shock and @entity295 .
