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Chronic Ethanol Administration Prevents Compensatory Cardiac Hypertrophy in Pressure Overload
Author(s) -
Ninh Van K.,
El Hajj Elia C.,
Mouton Alan J.,
El Hajj Milad C.,
Gilpin Nicholas W.,
Gardner Jason D.
Publication year - 2018
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.13799
Subject(s) - pressure overload , medicine , muscle hypertrophy , endocrinology , atrial natriuretic peptide , ventricular remodeling , volume overload , fibrosis , heart failure , extracellular matrix , ventricle , cardiology , chemistry , cardiac hypertrophy , biochemistry
Background Alcohol is among the most commonly abused drugs worldwide and affects many organ systems, including the heart. Alcoholic cardiomyopathy is characterized by a dilated cardiac phenotype with extensive hypertrophy and extracellular matrix ( ECM ) 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 ( PO ). Methods Abdominal aortic constriction was used to create PO in 8‐week‐old male Wistar rats. Alcohol administration was performed via chronic intermittent EtOH vapor inhalation for 2 weeks prior to surgery and for the duration of the 8‐week study. Echocardiography measurements were taken to assess ventricular functional and structural changes. Results PO increased posterior wall thickness and the hypertrophic markers, atrial and B‐type natriuretic peptides ( ANP and BNP ). With the added stressor of EtOH, wall thickness, ANP , and BNP decreased in PO animals. The combination of PO and EtOH resulted in increased wall stress compared to PO alone. PO also caused increased expression of collagen I and III , whereas EtOH alone only increased collagen III . The combined stresses of PO and EtOH led to an increase in collagen I expression, but collagen III did not change, resulting in an increased collagen I/ III ratio in the PO rats treated with EtOH. Lastly, Notch1 expression was significantly increased only in the PO rats treated with EtOH. Conclusions Our data indicate that chronic EtOH may limit the cardiac hypertrophy induced by PO which may be associated with a Notch1 mechanism, resulting in increased wall stress and altered ECM profile.