Satoru Ikenoue1,2,3, Feizal Waffarn1,2, Masanao Ohashi1,2,4, Mamoru Tanaka3, Daniel L Gillen5, Claudia Buss1,2,6, Sonja Entringer1,2,6, Pathik D Wadhwa1,2,7,8,9. 1. Development, Health and Disease Research Program, University of California, Irvine, Irvine, CA 92697, USA. 2. Department of Pediatrics, University of California, Irvine, Irvine, CA, USA. 3. Department of Obstetrics and Gynecology, Keio University School of Medicine, Tokyo, Japan. 4. Department of Obstetrics and Gynecology, University of Miyazaki, Miyazaki, Japan. 5. Department of Statistics, University of California, Irvine, Irvine, CA, USA. 6. Institute of Medical Psychology, Charité University Medicine, Berlin, Germany. 7. Department of Psychiatry and Human Behavior, University of California, Irvine, Irvine, CA, USA. 8. Department of Obstetrics and Gynecology, University of California, Irvine, Irvine, CA, USA. 9. Department of Epidemiology, University of California, Irvine, Irvine, CA, USA.
Abstract
CONTEXT: Variation in fetal liver blood flow influences fetal growth and postnatal body composition. Placental corticotrophin-releasing hormone has been implicated as a key mediator of placental-fetal perfusion. OBJECTIVE: To determine whether circulating levels of placental corticotrophin-releasing hormone across gestation are associated with variations in fetal liver blood flow. DESIGN: Prospective cohort study. METHODS: Fetal ultrasonography was performed at 30 weeks' gestation to characterize fetal liver blood flow (quantified by subtracting ductus venosus flow from umbilical vein flow). Placental corticotrophin-releasing hormone was measured in maternal circulation at approximately 12, 20, and 30 weeks' gestation. Multiple regression analysis was used to determine the proportion of variation in fetal liver blood flow explained by placental corticotrophin-releasing hormone. Covariates included maternal age, parity, pre-pregnancy body mass index, gestational weight gain, and fetal sex. RESULTS: A total of 79 uncomplicated singleton pregnancies were analyzed. Fetal liver blood flow was 68.4 ± 36.0 mL/min (mean ± SD). Placental corticotrophin-releasing hormone concentrations at 12, 20, and 30 weeks were 12.5 ± 8.1, 35.7 ± 24.5, and 247.9 ± 167.8 pg/mL, respectively. Placental corticotrophin-releasing hormone at 30 weeks, but not at 12 and 20 weeks, was significantly and positively associated with fetal liver blood flow at 30 weeks (r = 0.319; P = 0.004) and explained 10.4% of the variance in fetal liver blood flow. CONCLUSIONS: Placental corticotrophin-releasing hormone in late gestation is a possible modulator of fetal liver blood flow and may constitute a biochemical marker in clinical investigations of fetal growth and body composition.
CONTEXT: Variation in fetal liver blood flow influences fetal growth and postnatal body composition. Placental corticotrophin-releasing hormone has been implicated as a key mediator of placental-fetal perfusion. OBJECTIVE: To determine whether circulating levels of placental corticotrophin-releasing hormone across gestation are associated with variations in fetal liver blood flow. DESIGN: Prospective cohort study. METHODS: Fetal ultrasonography was performed at 30 weeks' gestation to characterize fetal liver blood flow (quantified by subtracting ductus venosus flow from umbilical vein flow). Placental corticotrophin-releasing hormone was measured in maternal circulation at approximately 12, 20, and 30 weeks' gestation. Multiple regression analysis was used to determine the proportion of variation in fetal liver blood flow explained by placental corticotrophin-releasing hormone. Covariates included maternal age, parity, pre-pregnancy body mass index, gestational weight gain, and fetal sex. RESULTS: A total of 79 uncomplicated singleton pregnancies were analyzed. Fetal liver blood flow was 68.4 ± 36.0 mL/min (mean ± SD). Placental corticotrophin-releasing hormone concentrations at 12, 20, and 30 weeks were 12.5 ± 8.1, 35.7 ± 24.5, and 247.9 ± 167.8 pg/mL, respectively. Placental corticotrophin-releasing hormone at 30 weeks, but not at 12 and 20 weeks, was significantly and positively associated with fetal liver blood flow at 30 weeks (r = 0.319; P = 0.004) and explained 10.4% of the variance in fetal liver blood flow. CONCLUSIONS: Placental corticotrophin-releasing hormone in late gestation is a possible modulator of fetal liver blood flow and may constitute a biochemical marker in clinical investigations of fetal growth and body composition.
Authors: Rui Adão; Pedro Mendes-Ferreira; Diana Santos-Ribeiro; Carolina Maia-Rocha; Luís D Pimentel; Cláudia Monteiro-Pinto; Eamon P Mulvaney; Helen M Reid; B Therese Kinsella; François Potus; Sandra Breuils-Bonnet; Miriam T Rademaker; Steeve Provencher; Sébastien Bonnet; Adelino F Leite-Moreira; Carmen Brás-Silva Journal: Cardiovasc Res Date: 2018-07-01 Impact factor: 10.787