Bhavisha A Bakrania1, Michael E Hall2, Sajid Shahul3, Joey P Granger4. 1. Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, United States. Electronic address: bbakrania@umc.edu. 2. Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, United States; Department of Medicine, University of Mississippi Medical Center, Jackson, MS, United States. 3. Department of Anesthesia and Critical Care, University of Chicago, Chicago, IL, United States. 4. Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, United States.
Abstract
BACKGROUND: Preeclampsia (PE) is a disorder prevalent in 3-8% of pregnancies, characterized by hypertension, endothelial dysfunction and cardiac dysfunction, including hypertrophy and impaired global longitudinal strain (GLS), which indicates reduced contractility and tissue injury. Despite several clinical studies highlighting impaired cardiac function in these women, the underlying mechanisms have not been studied, in part, due to lack of an appropriate animal model. The Reduced Uterine Perfusion Pressure (RUPP) rat model produces a PE-like phenotype, including adverse cardiac remodeling. However, whether this translates to impaired cardiac function is not known. The aim of this study was to test the hypothesis that placental ischemia in the RUPP rat leads to impaired left ventricular (LV) systolic function and GLS. STUDY DESIGN: RUPP (n = 10) rats underwent surgery to induce placental ischemia on gestational day (GD) 14. Sham (n = 10) and RUPP rats had indwelling carotid catheters placed on GD 18, and blood pressure and echocardiography measurements were made on GD 19. RESULTS: The RUPP group exhibited increased mean arterial pressure compared to the Sham group (123 ± 3 vs. 97 ± 2 mmHg, P < 0.01). RUPP hearts exhibited impaired LV ejection fraction (60 ± 2 vs. 78 ± 2%, P < 0.01) and GLS (-17.89 ± 0.5 vs. -26.31 ± 2.7%, P = 0.02), in addition to cardiac hypertrophy (0.97 ± 0.04 vs. 0.91 ± 0.02 g, P = 0.02). CONCLUSIONS: Cardiac dysfunction and impaired strain are present in RUPP rats during pregnancy. These findings represent an animal model of PE that could be used to understand the mechanisms of cardiac dysfunction in this disease and ultimately, improve or prevent cardiac abnormalities in these patients.
BACKGROUND: Preeclampsia (PE) is a disorder prevalent in 3-8% of pregnancies, characterized by hypertension, endothelial dysfunction and cardiac dysfunction, including hypertrophy and impaired global longitudinal strain (GLS), which indicates reduced contractility and tissue injury. Despite several clinical studies highlighting impaired cardiac function in these women, the underlying mechanisms have not been studied, in part, due to lack of an appropriate animal model. The Reduced Uterine Perfusion Pressure (RUPP) rat model produces a PE-like phenotype, including adverse cardiac remodeling. However, whether this translates to impaired cardiac function is not known. The aim of this study was to test the hypothesis that placental ischemia in the RUPP rat leads to impaired left ventricular (LV) systolic function and GLS. STUDY DESIGN: RUPP (n = 10) rats underwent surgery to induce placental ischemia on gestational day (GD) 14. Sham (n = 10) and RUPP rats had indwelling carotid catheters placed on GD 18, and blood pressure and echocardiography measurements were made on GD 19. RESULTS: The RUPP group exhibited increased mean arterial pressure compared to the Sham group (123 ± 3 vs. 97 ± 2 mmHg, P < 0.01). RUPP hearts exhibited impaired LV ejection fraction (60 ± 2 vs. 78 ± 2%, P < 0.01) and GLS (-17.89 ± 0.5 vs. -26.31 ± 2.7%, P = 0.02), in addition to cardiac hypertrophy (0.97 ± 0.04 vs. 0.91 ± 0.02 g, P = 0.02). CONCLUSIONS: Cardiac dysfunction and impaired strain are present in RUPP rats during pregnancy. These findings represent an animal model of PE that could be used to understand the mechanisms of cardiac dysfunction in this disease and ultimately, improve or prevent cardiac abnormalities in these patients.
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