Placental ischemia during pregnancy induces hypertension, cerebral inflammation, and oxidative stress in dams postpartum.

Background: Preeclampsia (PE) is characterized as de novo hypertension (HTN) with end-organ damage, especially in the brain. PE is hypothesized to be caused by placental ischemia. PE affects ~5-8% of USA pregnancies and increases the risk for HTN and cerebrovascular diseases (CVD) later in life.

Postpartum Dams Exposed to a Low-Resource Environment Display Neuroinflammation, Elevated Corticosterone, and Anhedonia-like Behavior.

Women living in an impoverished environment after birth have an increased risk of developing postpartum depression (PP-Dep) and hypertension (PP-HTN). The mechanisms underlying these heightened risks are unknown and understudied. To examine the relation between reduced environmental resources, PP-Dep, and PP-HTN; postpartum rodent dams were exposed to the low-resource limited bedding and nesting (LBN) chronic stress model during weaning.

Intrauterine growth-restricted pregnant rats, from placental ischemic dams, display preeclamptic-like symptoms: A new rat model of preeclampsia.

Preeclampsia (PE) is characterized by de novo hypertension (HTN) and is often associated with intrauterine growth restriction (IUGR). Hallmarks of PE are placental ischemia, decreased nitric oxide (NO) bioavailability, oxidative stress (OS), and organ damage in the kidneys and brain. This study aims to characterize a new model of PE using pregnant IUGR rats from hypertensive placental ischemic dams.