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

IF 1.8 4区 医学 Q3 PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH
Hsiu-Chu Chou, Chung-Ming Chen
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引用次数: 2

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.

子宫胎盘功能不全对生长受限新生大鼠心脏发育的影响。
胎儿生长受限(FGR)与新生儿心功能降低有关。子宫胎盘功能不全(UPI)是FGR最常见的原因。这些变化背后的机制尚不清楚。我们假设UPI会影响后代大鼠的心脏发育。通过本研究,我们评估了妊娠期UPI对生长受限新生大鼠心脏组织学和肺动脉高压的影响。妊娠第18天,采用双侧子宫血管结扎术(FGR组)或假手术(对照组)诱导UPI。在出生后第0天和第7天,取右肺中叶和心脏进行组织学和免疫组织化学评价。与对照组相比,FGR组在出生后第0天和第7天体重明显降低,心肌细胞肥大变性,心肌细胞和胶原沉积间隙增大,糖原沉积和HNK-1表达明显减少。这些结果表明,FGR新生儿可能心肌储备不足,这可能导致未来生活中心血管疾病的发生。需要进一步的研究来评估这些生长受限新生儿的血流动力学变化。
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来源期刊
Journal of Developmental Origins of Health and Disease
Journal of Developmental Origins of Health and Disease PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH-
CiteScore
3.80
自引率
0.00%
发文量
145
审稿时长
6-12 weeks
期刊介绍: JDOHaD publishes leading research in the field of Developmental Origins of Health and Disease (DOHaD). The Journal focuses on the environment during early pre-natal and post-natal animal and human development, interactions between environmental and genetic factors, including environmental toxicants, and their influence on health and disease risk throughout the lifespan. JDOHaD publishes work on developmental programming, fetal and neonatal biology and physiology, early life nutrition, especially during the first 1,000 days of life, human ecology and evolution and Gene-Environment Interactions. JDOHaD also accepts manuscripts that address the social determinants or education of health and disease risk as they relate to the early life period, as well as the economic and health care costs of a poor start to life. Accordingly, JDOHaD is multi-disciplinary, with contributions from basic scientists working in the fields of physiology, biochemistry and nutrition, endocrinology and metabolism, developmental biology, molecular biology/ epigenetics, human biology/ anthropology, and evolutionary developmental biology. Moreover clinicians, nutritionists, epidemiologists, social scientists, economists, public health specialists and policy makers are very welcome to submit manuscripts. The journal includes original research articles, short communications and reviews, and has regular themed issues, with guest editors; it is also a platform for conference/workshop reports, and for opinion, comment and interaction.
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