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Updated: Aug 25, 2025
Fetal Echocardiography and Pulsed-wave Doppler Ultrasound in a Rabbit Model of Intrauterine Growth Restriction
Published on: June 29, 2013
Effects of uteroplacental insufficiency on cardiac development in growth-restricted newborn rats
Hsiu-Chu Chou1, Chung-Ming Chen2,3
1Department of Anatomy and Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Insights
Uteroplacental insufficiency (UPI) in pregnant rats led to fetal growth restriction (FGR) in newborns, causing heart muscle damage and potential long-term cardiovascular issues.
Area of Science:
- Cardiovascular Biology
- Developmental Biology
- Neonatal Physiology
Background:
- Fetal growth restriction (FGR) is linked to impaired neonatal cardiac function.
- Uteroplacental insufficiency (UPI) is a primary cause of FGR, but its impact on cardiac development is not fully understood.
Purpose of the Study:
- To investigate the effects of UPI-induced FGR on heart histology and pulmonary hypertension in newborn rats.
Main Methods:
- UPI was induced via bilateral uterine vessel ligation in pregnant rats on gestation Day 18.
- Control group underwent sham surgery.
- Heart and lung tissues were collected on postnatal days 0 and 7 for histological and immunohistochemical analysis.
Main Results:
- FGR neonates showed significantly lower body weight compared to controls.
- Histological examination revealed cardiomyocyte hypertrophy, degeneration, increased intercellular spaces, and collagen deposition in FGR neonates.
- Reduced glycogen deposition and HNK-1 expression were observed in the FGR group.
Conclusions:
- UPI-induced FGR negatively impacts cardiac development in rat neonates.
- These cardiac alterations suggest inadequate myocardial reserves, potentially leading to future cardiovascular compromise.
- Further research is needed to explore hemodynamic changes in growth-restricted neonates.
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.
