Women who develop preeclampsia during pregnancy are more likely to develop cardiovascular disease later in life, even if they are otherwise healthy. The reason why this occurs is unclear but may be related to blood vessel damage and increased inflammation that occurs during the preeclamptic pregnancy and persists postpartum. The purpose of this investigation is to 1) determine the mechanisms contributing to this lasting blood vessel damage and chronic inflammation, and to 2) identify factors (both physiological and pharmacological) that mitigate these negative effects in order to inform better clinical management of cardiovascular disease risk in women who have had preeclampsia.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
TRIPLE
Enrollment
24
1500mg twice daily for 4 days prior to experimental testing
Placebo oral table twice daily for 4 days prior to experimental testing
University of Iowa
Iowa City, Iowa, United States
Pennsylvania State University
University Park, Pennsylvania, United States
Microvascular Endothelial Function (Cutaneous Conductance, %Maximum)
Endothelium-dependent vasodilation assessed as cutaneous conductance response (cutaneous conductance = local red blood cell flux/mean arterial pressure; %maximum) to exogenous acetylcholine delivered via intradermal microdialysis.
Time frame: immediately following the 4 days or oral treatment (salsalate or placebo)
Peripheral Blood Mononuclear Cell Inflammatory Response to Ang II
inflammatory cytokine (TNFalpha) release by peripheral blood mononuclear cells isolated from fresh whole blood collected via venipuncture and stimulated with angiotensin II ex vivo.
Time frame: at the completion of 4 days of oral (placebo or salsalate) treatment
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