Reduced utero‐placental perfusion results in placental ischemia, an initiating event in the pathophysiology of preeclampsia, a hypertensive disorder of pregnancy. There is evidence that women with a history of preeclampsia have increased risk of mortality from Alzheimer's disease, stroke, and cerebrovascular complications years after delivery; however, the underlying mechanisms are not known. Additionally, pre‐clinical studies demonstrate that during pregnancy, placental ischemia, induced by reducing uterine perfusion pressure (RUPP), leads to cerebral edema and increased blood‐brain barrier (BBB) permeability; however, it is not known whether these complications persist after delivery. In this study, we tested the hypothesis that placental ischemia contributes to cerebrovascular abnormalities postpartum. On gestational day 14, time‐pregnant Sprague Dawley rats underwent sham or RUPP surgery (n = 5 per group) and brains were collected 2 months postpartum. Cerebral edema, assessed by measuring water content, was observed in the posterior cortex following RUPP with no significant changes in the anterior cerebrum, hippocampus, or striatum. Using a rat cytokine/chemokine multi‐plex kit, we found a shift towards a pro‐inflammatory environment in the posterior cortex with increases in IL‐17, IL‐1α, and IL‐1β. In the hippocampus, where brain water content was unchanged, IL‐4 increased and IL‐18 decreased following RUPP. Western blot analysis showed no changes in the astrocyte marker, Glial Fibrillary Acidic Protein (GFAP); however, the microglia marker, ionized calcium binding adaptor molecule (Iba1) tended to increase in the hippocampus of RUPP‐exposed rats (p=0.05). There was no change in hippocampal or posterior cortical expression of the blood‐brain barrier associated proteins, Claudin‐1, zonular occludens (ZO‐1), or Aquaporin‐4 (AQP4); however, posterior cortical occludin was significantly reduced in RUPP‐exposed rats. These results suggest that at 2 months postpartum, a pro‐inflammatory environment in the posterior cortex is associated with tissue edema. Our results support the hypothesis that placental ischemia leads to sustained inflammation and reduced blood‐brain barrier integrity that predispose exposed moms to edema in brain regions important for learning and memory. Whether these findings are exacerbated with increased time after delivery is an area of active investigation.Support or Funding InformationNIH K99/R00HL129192, COBRE Pilot Grant, P20GM104357, P01HL051971, R25HL121042This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.