A Rodent Model of Alcoholic Heart Muscle Disease and Its Evaluation by Echocardiography

Abstract

Transthoracic echocardiography was used in a rodent animal model to determine whether long-term alcohol consumption (8 and 12 months) was associated with the development of a dilated cardiomyopathy. We also investigated whether alcohol-induced changes in cardiac structure corresponded to activation of the renin-angiotensin system and the natriuretic peptide (NP) system. Male rats received either the Lieber-DeCarli liquid alcohol diet (EtOH) (9%v/v) (n = 8) or control diet (CON) (n = 8). Echocardiography (echo) was used to determine left-ventricular (LV) dimensions, and isolated heart studies (Langendorff and atrium) were used to assess ex vivo contractility. Plasma and tissue angiotensin-I converting enzyme (ACE) activity was measured. Gene expression, plasma, and tissue levels of the NPs were determined by northern blot analysis and radioimmunoassay, respectively. After 8 months of alcohol consumption, there was a trend for the end diastolic dimension, end systolic dimension, and LV mass to be greater in the 8 month EtOH group compared with the CON group. However, after 12 months of alcohol consumption, significant increases were found between the groups in several echo parameters. Tissue ACE activity (nmoles/min/mg protein) was greater in the 12 month EtOH group compared with the 12 month CON and 8 month EtOH group (p < 0.05). We found no differences between groups in gene expression (messenger RNA), plasma, and tissue levels of the NPs. Echocardiography revealed that 8 to 12 months of alcohol consumption was associated with the development of a dilated cardiomyopathy. However, this was not preceded by an increase in tissue ACE activity, and these changes occurred in the absence of increased plasma and LV tissue levels of the NPs.