Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, United States.
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.
Pregnancy Hypertens. 2019 Oct;18:169-172. doi: 10.1016/j.preghy.2019.10.001. Epub 2019 Oct 24.
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.
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.
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).
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.
子痫前期(PE)是一种在 3-8%的妊娠中普遍存在的疾病,其特征是高血压、内皮功能障碍和心脏功能障碍,包括心肌肥厚和整体纵向应变(GLS)受损,这表明收缩力降低和组织损伤。尽管有几项临床研究强调了这些女性的心脏功能受损,但由于缺乏合适的动物模型,其潜在机制尚未得到研究。减少子宫灌注压(RUPP)大鼠模型产生类似 PE 的表型,包括心脏不良重构。然而,这是否转化为心脏功能受损尚不清楚。本研究旨在检验假设,即 RUPP 大鼠的胎盘缺血导致左心室(LV)收缩功能和 GLS 受损。
RUPP(n=10)大鼠在妊娠第 14 天接受手术诱导胎盘缺血。假手术(n=10)和 RUPP 大鼠在妊娠第 18 天放置颈内导管,并在妊娠第 19 天进行血压和超声心动图测量。
与假手术组相比,RUPP 组的平均动脉压升高(123±3 对 97±2mmHg,P<0.01)。RUPP 心脏表现出 LV 射血分数受损(60±2 对 78±2%,P<0.01)和 GLS 降低(-17.89±0.5 对-26.31±2.7%,P=0.02),此外还有心脏肥大(0.97±0.04 对 0.91±0.02g,P=0.02)。
在妊娠期间,RUPP 大鼠存在心脏功能障碍和应变受损。这些发现代表了一种 PE 动物模型,可用于了解该疾病中心脏功能障碍的机制,并最终改善或预防这些患者的心脏异常。