XXXX Inhibition by HET0016 Offers Neuroprotection, Decreases @entity4 , and Increases Cortical Cerebral Blood Flow in a Pediatric Asphyxial Cardiac Arrest Model in @entity35 .

@entity4 @entity15759 @entity51 @entity179 @entity1167 @entity35 @entity1813 @entity1779
Vasoconstrictive and vasodilatory @entity1813 generated after @entity1167 ( @entity1167 ) may contribute to cerebral vasomotor disturbances and @entity179 . We evaluated the balance of vasodilator/vasoconstrictor @entity1813 produced by cytochrome P450 (CYP) metabolism, and determined their role on cortical perfusion, functional outcome, and @entity179 after pediatric asphyxial @entity1167 . @entity1167 of 9 and 12 minutes was induced in 16- to 18-day-old @entity35 . At 5 and 120 minutes after @entity1167 , we quantified the concentration of CYP @entity1813 in the cortex and subcortical areas. In separate @entity35 , we inhibited @entity15759 ( @entity15759 ) synthesis after @entity1167 and assessed cortical cerebral blood flow (CBF), @entity51 score, @entity179 , and @entity4 . After 9 minutes of @entity1167 , vasodilator @entity1813 markedly increased versus sham. Conversely, after 12 minutes of @entity1167 , vasoconstrictor eicosanoid @entity15759 increased versus sham, without compensatory increases in vasodilator @entity1813 . Inhibition of @entity15759 synthesis after 12 minutes of @entity1167 decreased cortical @entity15759 levels, increased CBF, reduced @entity51 at 3 hours, and reduced @entity179 and @entity4 at 48 hours versus vehicle-treated @entity35 . In conclusion, cerebral vasoconstrictor @entity1813 increased after a pediatric @entity1167 of 12 minutes. Inhibition of @entity15759 synthesis improved cortical perfusion and short-term neurologic outcome. These results suggest that alterations in CYP @entity1813 have a role in @entity1779 and @entity179 after @entity1167 and may represent important therapeutic targets.
