{"title":"子宫胎盘功能不全对生长受限新生大鼠心脏发育的影响。","authors":"Hsiu-Chu Chou, Chung-Ming Chen","doi":"10.1017/S2040174422000575","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"14 2","pages":"272-278"},"PeriodicalIF":1.8000,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"Effects of uteroplacental insufficiency on cardiac development in growth-restricted newborn rats.\",\"authors\":\"Hsiu-Chu Chou, Chung-Ming Chen\",\"doi\":\"10.1017/S2040174422000575\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":49167,\"journal\":{\"name\":\"Journal of Developmental Origins of Health and Disease\",\"volume\":\"14 2\",\"pages\":\"272-278\"},\"PeriodicalIF\":1.8000,\"publicationDate\":\"2023-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Developmental Origins of Health and Disease\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1017/S2040174422000575\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Developmental Origins of Health and Disease","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1017/S2040174422000575","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH","Score":null,"Total":0}
Effects of uteroplacental insufficiency on cardiac development in growth-restricted newborn rats.
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.
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.