Abstract 20787: Maternal Obesity Causes Contractile Dysfunction of Term Fetal Sheep Cardiomyocytes
Background: Maternal obesity (MO), in pregnancy, predisposes offspring to a higher risk of obesity, heart disease, hypertension, and vascular dysfunction, known as fetal programming. However, the effect of MO on contractile function of fetal cardiomyocytes has not been studied. We assessed contractile function in cardiomyocytes of fetuses of MO and control normal weight sheep at term.
Methods: From 60 days before and throughout pregnancy, Rambouillet/Columbia crossed ewes were fed either 100% of National Research Council (NRC) recommendations (control, n=8) or 150% of NRC’s recommendations (MO, n=7). At 135 day gestation (Term 150 days), pregnant ewes and fetuses underwent general anesthesia. The fetal heart was quickly removed and perfused to isolate cardiomyocytes. Contractile and intracellular Ca2+ properties were evaluated using an IonOptix system. Analysis by Student’s t-test: p < 0.05.
Results: MO elevated maternal body weight, total heart and cardiac ventricular weights and wall thicknesses (p < 0.05). Fetuses from MO ewes had greater body weight and left ventricular (LV) weight (p < 0.05). LV and right ventricle (RV) cardiomyocytes from fetuses of MO ewes showed increased cell length and decreased peak shortening. LV cardiomyocytes showed decreased sarcomere length (p < 0.05). MO disrupted fetal cardiomyocyte intracellular Ca2+ homeostasis, evidenced by increased resting and peak intracellular Ca2+ levels in LV and RV fetal cardiomyocytes (p < 0.05).
Conclusions: MO impairs fetal cardiac morphometry and contractile function. To our knowledge this is the first study to evaluate functional properties in cardiomyocytes of fetuses of obese mothers providing potential mechanisms for programming of later life cardiac disease.
Author Disclosures: Q. Wang: None. C. Zhu: None. M. Sun: None. N. Hu: None. S.P. Ford: None. P.W. Nathanielsz: None. J. Ren: None. W. Guo: None.
- © 2016 by American Heart Association, Inc.