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Alcoholic cardiomyopathy is characterized by a dilated cardiac phenotype with extensive hypertrophy and extracellular matrix (<jats:styled-content style=\"fixed-case\">ECM<\/jats:styled-content>) remodeling. We have previously shown that chronic ethanol (EtOH) administration accelerates the progression to heart failure in a rat model of volume overload. However, the mechanism by which this decompensation occurs is unknown. For this study, we hypothesized that chronic EtOH administration would prevent compensatory hypertrophy and cardiac remodeling in a rodent model of pressure overload (<jats:styled-content style=\"fixed-case\">PO<\/jats:styled-content>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Abdominal aortic constriction was used to create <jats:styled-content style=\"fixed-case\">PO<\/jats:styled-content> in 8\u2010week\u2010old male Wistar rats. Alcohol administration was performed via chronic intermittent EtOH vapor inhalation for 2\u00a0weeks prior to surgery and for the duration of the 8\u2010week study. Echocardiography measurements were taken to assess ventricular functional and structural changes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>PO increased posterior wall thickness and the hypertrophic markers, atrial and B\u2010type natriuretic peptides (<jats:styled-content style=\"fixed-case\">ANP<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">BNP<\/jats:styled-content>). With the added stressor of EtOH, wall thickness, <jats:styled-content style=\"fixed-case\">ANP<\/jats:styled-content>, and <jats:styled-content style=\"fixed-case\">BNP<\/jats:styled-content> decreased in <jats:styled-content style=\"fixed-case\">PO<\/jats:styled-content> animals. The combination of <jats:styled-content style=\"fixed-case\">PO<\/jats:styled-content> and EtOH resulted in increased wall stress compared to <jats:styled-content style=\"fixed-case\">PO<\/jats:styled-content> alone. <jats:styled-content style=\"fixed-case\">PO<\/jats:styled-content> also caused increased expression of collagen I and <jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>, whereas EtOH alone only increased collagen <jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>. The combined stresses of <jats:styled-content style=\"fixed-case\">PO<\/jats:styled-content> and EtOH led to an increase in collagen I expression, but collagen <jats:styled-content style=\"fixed-case\">III<\/jats:styled-content> did not change, resulting in an increased collagen I\/<jats:styled-content style=\"fixed-case\">III<\/jats:styled-content> ratio in the <jats:styled-content style=\"fixed-case\">PO<\/jats:styled-content> rats treated with EtOH. Lastly, Notch1 expression was significantly increased only in the <jats:styled-content style=\"fixed-case\">PO<\/jats:styled-content> rats treated with EtOH.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Our data indicate that chronic EtOH may limit the cardiac hypertrophy induced by <jats:styled-content style=\"fixed-case\">PO<\/jats:styled-content> which may be associated with a Notch1 mechanism, resulting in increased wall stress and altered <jats:styled-content style=\"fixed-case\">ECM<\/jats:styled-content> profile.<\/jats:p><\/jats:sec>","DOI":"10.1111\/acer.13799","type":"journal-article","created":{"date-parts":[[2018,5,30]],"date-time":"2018-05-30T12:50:07Z","timestamp":1527684607000},"page":"1408-1417","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Chronic Ethanol Administration Prevents Compensatory Cardiac Hypertrophy in Pressure Overload"],"prefix":"10.1111","volume":"42","author":[{"given":"Van K.","family":"Ninh","sequence":"first","affiliation":[{"name":"Department of Physiology LSU Health Sciences Center New Orleans Louisiana"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elia C.","family":"El Hajj","sequence":"additional","affiliation":[{"name":"Department of Physiology LSU Health Sciences Center New Orleans Louisiana"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alan J.","family":"Mouton","sequence":"additional","affiliation":[{"name":"Department of Physiology LSU Health Sciences Center New Orleans Louisiana"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Milad C.","family":"El Hajj","sequence":"additional","affiliation":[{"name":"Department of Physiology LSU Health Sciences Center New Orleans Louisiana"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholas W.","family":"Gilpin","sequence":"additional","affiliation":[{"name":"Department of Physiology LSU Health Sciences Center New Orleans Louisiana"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4785-7357","authenticated-orcid":false,"given":"Jason D.","family":"Gardner","sequence":"additional","affiliation":[{"name":"Department of Physiology LSU Health Sciences Center New Orleans Louisiana"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2018,6,13]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1210\/er.2006-0046"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1186\/scrt190"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/0012-1606(83)90098-2"},{"key":"e_1_2_7_5_1","first-page":"333","article-title":"Myocardial characteristics of pressure overload hypertrophy. 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