Citation

Andersson BS, Rajs J, Sundberg M, Sótonyi P, Lind B. J. Stud. Alcohol 1995; 56(2): 147-155.

Affiliation

Department of Forensic Medicine, Karolinska Institute, Stockholm, Sweden.

Copyright

(Copyright © 1995, Rutgers Center of Alcohol Studies)

DOI

unavailable

PMID

7760559

Abstract

OBJECTIVE: It has been shown that chronic consumption of ethanol can impair myocardial function and result in morphological changes of the heart. The purpose of this work was to evaluate relations between changes in energy metabolism and changes of cell morphology. METHOD: Long-term effects of moderate ethanol consumption on the heart were examined in isolated cardiomyocytes from rats fed a pellet with low-protein content for 6 months. Digitonin treatment of the cardiomyocytes was used to separate mitochondrial and cytosolic fractions. RESULTS: A greater fraction of contracted myocytes was isolated from ethanol- and glucose-treated rats, than from rats fed only glucose and/or water as liquid supplement. There were changes of the ultrastructure of myocytes from ethanol and glucose-treated rats, which included mitochondrial degeneration, accumulation of fat droplets and depletion of the glycogen content. An elevated cytosolic level of nucleotides (ATP, ADP and NAD) and disappearance of magnesium from the mitochondrial fraction were observed in myocytes from rats fed ethanol and glucose. The release of adenosine was also found to be inhibited in these cells. CONCLUSIONS: Our results show that moderate ethanol consumption by rats during protein-restricted conditions produces subclinical changes of cardiomyocyte ultrastructure and alteration of cell morphology. Furthermore, the results indicate that changes of the energy homeostasis in myocytes and inhibition of sarcolemmal adenosine transport are early events that appear to precede the histological alterations.

Language: en