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Research Article Free access | 10.1172/JCI107812

Myocardial Function and Lipid Metabolism in the Chronic Alcoholic Animal

Timothy J. Regan, Mohammad I. Khan, Philip O. Ettinger, Bunyad Haider, Michael M. Lyons, Henry A. Oldewurtel, and Marilyn Weber

1From the Department of Medicine, College of Medicine and Dentistry-New Jersey Medical School, Newark, New Jersey 07103

Find articles by Regan, T. in: PubMed | Google Scholar

1From the Department of Medicine, College of Medicine and Dentistry-New Jersey Medical School, Newark, New Jersey 07103

Find articles by Khan, M. in: PubMed | Google Scholar

1From the Department of Medicine, College of Medicine and Dentistry-New Jersey Medical School, Newark, New Jersey 07103

Find articles by Ettinger, P. in: PubMed | Google Scholar

1From the Department of Medicine, College of Medicine and Dentistry-New Jersey Medical School, Newark, New Jersey 07103

Find articles by Haider, B. in: PubMed | Google Scholar

1From the Department of Medicine, College of Medicine and Dentistry-New Jersey Medical School, Newark, New Jersey 07103

Find articles by Lyons, M. in: PubMed | Google Scholar

1From the Department of Medicine, College of Medicine and Dentistry-New Jersey Medical School, Newark, New Jersey 07103

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1From the Department of Medicine, College of Medicine and Dentistry-New Jersey Medical School, Newark, New Jersey 07103

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Published September 1, 1974 - More info

Published in Volume 54, Issue 3 on September 1, 1974
J Clin Invest. 1974;54(3):740–752. https://doi.org/10.1172/JCI107812.
© 1974 The American Society for Clinical Investigation
Published September 1, 1974 - Version history
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Abstract

In view of the variables that obscure the pathogenesis of cardiomyopathy, a study was undertaken in mongrel dogs fed ethanol as 36% of calories for up to 22 mo. Both the experimental and control groups maintained body weight, hematocrit, plasma vitamin, and protein levels. Left ventricular function was evaluated in the intact anesthetized dog using indicator dilution for end-diastolic and stroke volume determinations. During increased afterload with angiotensin, the ethanol group exhibited a larger rise of end-diastolic pressure (P<0.01), whereas end-diastolic and stroke volume responses were significantly less than in controls. Preload increments with saline elicited a significantly higher end-diastolic pressure rise in the ethanol group (P<0.01). No hypertrophy, inflammation, or fibrosis was present and it was postulated that the enhanced diastolic stiffness was related to accumulation of Alcian Blue-positive material in the ventricular interstitium.

To evaluate myocardial lipid metabolism, [1-14C]oleic acid was infused systemically. Plasma specific activity and myocardial lipid uptake were similar in both groups. There was a significantly increased incorporation of label into triglyceride, associated with a reduced 14CO2 production, considered the basis for a twofold increment of triglyceride content. In addition, diminished incorporation of [14C]oleic acid into phospholipid was observed accompanied by morphologic abnormalities of cardiac cell membranes. Potassium loss and sodium gain, like the lipid alteration, was more prominent in the subendocardium. Thus, chronic ethanol ingestion in this animal model is associated with abnormalities of ventricular function without evident malnutrition, analogous to the preclinical malfunction described in the human alcoholic.

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