Low‐dose maternal alcohol consumption: effects in the hearts of offspring in early life and adulthood. Issue 7 (July 2014)

• Record Type: Journal Article
• Authors: Nguyen, Vivian B.; Probyn, Megan E.; Campbell, Fiona; Yin, Kom V.; Samuel, Chrishan S.; Zimanyi, Monika A.; Bertram, John F.; Black, Mary Jane; Moritz, Karen M.
• Is Part Of: Physiological reports. Volume 2:Issue 7(2014:Jul.)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2014-07
• Subjects: Physiology -- Periodicals; 571
• DOI: 10.14814/phy2.12087
• Languages: English
• ISSNs: 2051-817X

Abstract

<abstract abstract-type="main" id="phy212087-abs-0001"> <title>Abstract</title> <p>High alcohol consumption during pregnancy leads to deleterious effects on fetal cardiac structure and it also affects cardiomyocyte growth and maturation. This study aimed to determine whether low levels of maternal alcohol consumption are also detrimental to cardiomyocyte and cardiac growth in the early life of offspring and whether cardiac structure and function in adulthood is affected. Pregnant Sprague–Dawley rat dams were fed a control or 6% (volume/volume) liquid‐based ethanol supplemented (isocaloric) diet throughout gestation. At embryonic day 20, the expression of genes involved in cardiac development was analyzed using Real‐time PCR. At postnatal day 30, cardiomyocyte number, size, and nuclearity in the left ventricle (LV) were determined stereologically. In 8‐month‐old offspring, LV fibrosis and cardiac function (by echocardiography) were examined. Maternal ethanol consumption did not alter gene expression of the cardiac growth factors in the fetus or cardiomyocyte number in weanling offspring. However, at 8 months, there were significant increases in LV anterior and posterior wall thickness during diastole in ethanol‐exposed offspring (<italic>P </italic>= 0.037 and <italic>P </italic>= 0.024, respectively), indicative of left ventricular hypertrophy; this was accompanied by a significant increase in fibrosis. Additionally, maximal aortic flow velocity was significantly decreased in ethanol‐exposed offspring (<italic>P </italic>= 0.035). In conclusion, although there were no detectable early‐life differences in cardiac and cardiomyocyte growth in animals exposed to a chronic low dose of ethanol during gestation, there were clearly deleterious outcomes by adulthood. This suggests that even relatively low doses of alcohol consumed during pregnancy can be detrimental to long‐term cardiac health in the offspring.</p> </abstract>