Exposure to placental ischemia impairs postpartum maternal renal and cardiac function in rats
Nina D Paauw, Jaap A Joles, Frank T Spradley, Bhavisha Bakrania, Zsuzsanna K Zellenger, Arie Franx, Marianne C Verhaar, Joey P Granger, A Titia LelyAmerican Journal of Physiology - Regulatory, Integrative and Comparative Physiology2017
INTRODUCTION: Women with a history of preeclampsia (PE) have an increased risk to develop cardiovascular and renal diseases later in life, but the mechanisms underlying this effect are unknown. In rats, we assessed whether placental ischemia results in long-term effects on the maternal cardiovascular and renal systems using the Reduced Uterine Perfusion Pressure (RUPP) model for PE. METHODS: Sprague-Dawley rats received either a SHAM or RUPP operation at gestational day 14. The rats were followed for eight weeks after delivery (SHAM n=12, RUPP n=21) at which time mean arterial pressure (MAP; conscious), 24-hour albuminuria, GFR (transcutaneous, FITC-sinistrin), and cardiac function (Vevo 770 system) were assessed. Subsequently, all rats were sacrificed for mesenteric artery vasorelaxation and histology of heart and kidney. RESULTS: At eight weeks after delivery, there was no difference in MAP and albuminuria. However, RUPP rats showed a significantly reduced GFR [2.61 +/- 0.53 vs 3.37 +/- 0.74ml/min; p=0.01]. Ultrasound showed comparable cardiac structure, but RUPP rats had a lower left ventricular ejection fraction (62 +/- 7 vs 69 +/- 10%; p=0.04). Heart and kidney histology was not different between SHAM or RUPP rats. Furthermore, there were no differences in endothelial dependent or independent vasorelaxation. CONCLUSIONS: We show that exposure to placental ischemia in rats is accompanied by functional disturbances in maternal renal and cardiac function eight weeks after a preeclamptic pregnancy. However, these changes were not dependent on differences in blood pressure, small artery vasorelaxation, or cardiac and renal structure at this time point postpartum.