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Effects of uteroplacental insufficiency on cardiac development in growth-restricted newborn rats

Published online by Cambridge University Press:  14 October 2022

Hsiu-Chu Chou
Affiliation:
Department of Anatomy and Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
Chung-Ming Chen*
Affiliation:
Department of Pediatrics, Taipei Medical University Hospital, Taipei, Taiwan Department of Pediatrics, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
*
Address for correspondence: Chung-Ming Chen, Department of Pediatrics, Taipei Medical University Hospital, Taipei 110, Taiwan. Email: cmchen@tmu.edu.tw

Abstract

Fetal growth restriction (FGR) is associated with reduced cardiac function in neonates. Uteroplacental insufficiency (UPI) is the most common cause of FGR. The mechanisms underlying these alterations remain unknown. We hypothesized that UPI would influence cardiac development in offspring rats. Through this study, we evaluated the effects of UPI during pregnancy on heart histology and pulmonary hypertension in growth-restricted newborn rats. On gestation Day 18, either UPI was induced through bilateral uterine vessel ligation (FGR group) or sham surgery (control group) was performed. The right middle lobe of the lung and the heart were harvested for histological and immunohistochemical evaluation on postnatal days 0 and 7. The FGR group exhibited significantly lower body weight, hypertrophy and degeneration of cardiomyocytes, increased intercellular spaces between the cardiomyocytes and collagen deposition, and decreased glycogen deposition and HNK-1 expression compared with the control group on postnatal days 0 and 7. These results suggest that neonates with FGR may have inadequate myocardial reserves, which may cause subsequent cardiovascular compromise in future life. Further studies are required to evaluate the hemodynamic changes in these growth-restricted neonates.

Type
Original Article
Copyright
© The Author(s), 2022. Published by Cambridge University Press in association with International Society for Developmental Origins of Health and Disease

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