Long- and short-term alcohol consumption induce a variety of cardiovascular changes, including alterations in hemodynamic variables and tissue biochemistry. In many instances some of the perturbations may be considered as compensatory adjustments, and indeed, there is some controversy that moderate long-term consumption may cause alterations in plasma lipid profiles, conferring cardiovascular protection by reducing the incidence of coronary artery disease. In the long term, however, ethanol misuse may induce a specific disease entity, namely alcoholic heart muscle disease, and short-term ethanol exposure may also perturb tissue contractility and hemodynamic indices. The mechanisms of these changes are unknown, but central to many of the metabolic and functional disturbances are alterations in tissue protein synthesis, perhaps precipitated or exacerbated by free radial formation or by the formation of protein-acetaldehyde adducts. Methods for measuring protein synthesis in vivo are reviewed, and their application to elucidating the mechanisms involved in cardiac abnormalities is described, including the effects of ethanol. Our results demonstrate that the effects of alcohol toxicity also occur at the subcellular level, and the synthesis of mitochondrial proteins are reduced in vivo, perhaps even contribution to defects in energy generation, the normal function of which is required to maintain contractility.