Changes in cerebral inflammation and blood pressure in postpartum preeclamptic rats




Wiemann, Natalia
Smith, Jonna
Smith, Savanna
Jones, Kylie
Castillo, Angie
Cromartie, Whitney
Owen, Malissa
McCafferty, Adair
Srivastava, Prakriti
Cunningham, Mark


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Introduction: Postpartum (PP) preeclamptic (PE) women have an increased risk of developing hypertension (HTN) and cerebrovascular diseases later in life. Studies show that women who experience preeclampsia go on to develop HTN 7-8 years earlier than women with normal pregnancies, increasing their risk for developing cerebrovascular diseases such as stroke. While the timing and mechanisms contributing to a rise in blood pressure (BP) and cerebrovascular dysfunction in postpartum preeclamptic women are unknown, they are hypothesized to be influenced by inflammation. Previous studies in our lab indicate postpartum PE rats at 10 weeks have HTN and increased inflammation (PMID: 34727994). Our current study will examine BP and inflammation in postpartum PE rats at an earlier time point, 6 weeks (PP6), to determine the relationship between cerebral inflammation and the pathophysiology of HTN. We hypothesize that postpartum PE rats will have an increase in BP and cerebral inflammation 6 weeks after delivery. Methods: Pregnant Sprague Dawley rats were divided into 2 groups: normal pregnant (NP) rats, and preeclamptic (RUPP) rats. Placental ischemia was surgically induced in the preeclamptic group via the reduced uterine perfusion pressure (RUPP) model. All rats gave birth naturally and were weaned for 3 weeks. At PP6, BP was measured via carotid catheterization, and brain tissue was collected to measure pro-inflammatory (TNF-α and IL-17) and anti-inflammatory (IL-4 and IL-10) factors via colorimetric assays and ELISAs. Results: Blood pressure was elevated in RUPP PP vs NP PP (128±6 vs 106±4mmHg, p<0.05). Cerebral TNF-α drastically increased by ~2.4 fold in RUPP PP vs NP PP (2576±445.6 vs 1058±212.5pg/mL, ns). Cerebral IL-17(331.2±41.1 vs 297.6±48.6pg/mL, ns) and IL-4 (178.4±23.4 vs 154.8±14pg/mL, ns) also increased in RUPP PP vs NP PP. Cerebral IL-10 (103.9±21.4 vs 147.6±11.3pg/mL, ns) was decreased in RUPP PP vs NP PP rats. Conclusion: PP6 preeclamptic rats have HTN and increased cerebral inflammation. It is yet to be determined whether cerebral inflammatory markers are the cause or consequence of HTN in PP6 PE rats. Future studies will explore the sequence of HTN and cerebral inflammation in postpartum PE rats and determine how brain inflammation contributes to HTN and cerebral damage. We will also target specific areas of the brain that modulate autonomic function and BP. This study is clinically relevant because it will inform providers on the pathophysiology of HTN and/or cerebral damage in women after a PE pregnancy. Our findings suggest that the use of inflammatory therapeutic targets improves HTN and cerebrovascular dysfunction in postpartum PE women.