BACKGROUND: Excessive alcohol consumption is recognized as a common cause of left ventricular (LV) dysfunction. It is currently thought that 36% of all cases of dilated cardiomyopathy are due to excessive alcohol intake. Suitable animal models are needed to study the pathogenic mechanisms of ethanol-induced LV dysfunction. We have therefore created a new model of ethanol-induced LV dysfunction in the chicken. METHODS: For 12 weeks, adult chickens were given, twice a day, by gavage, 73% of their total calculated daily water intake containing a 20% ethanol concentration. Twenty percent ethanol also was placed in the water and provided ad libitum. Control chickens received the same volume of water by gavage twice a day without ethanol. Water without ethanol was given ad libitum to control birds. RESULTS: Our study shows that after a relatively short duration of ethanol ingestion, chickens developed LV dilatation and LV dysfunction. The serum concentrations of ethanol attained in this new model were similar to those reported in humans. Furthermore, unlike other currently available animal models of ethanol-induced cardiac disease, this model demonstrates myocyte hypertrophy, interstitial fibrosis, and myocytolysis, similar to observations in human ethanol-induced cardiac dysfunction. CONCLUSIONS: We conclude that this new avian model should provide a useful tool for investigating the mechanism(s) and pathophysiology of ethanol-induced dilated cardiomyopathy and heart failure.
BACKGROUND: Excessive alcohol consumption is recognized as a common cause of left ventricular (LV) dysfunction. It is currently thought that 36% of all cases of dilated cardiomyopathy are due to excessive alcohol intake. Suitable animal models are needed to study the pathogenic mechanisms of ethanol-induced LV dysfunction. We have therefore created a new model of ethanol-induced LV dysfunction in the chicken. METHODS: For 12 weeks, adult chickens were given, twice a day, by gavage, 73% of their total calculated daily water intake containing a 20% ethanol concentration. Twenty percent ethanol also was placed in the water and provided ad libitum. Control chickens received the same volume of water by gavage twice a day without ethanol. Water without ethanol was given ad libitum to control birds. RESULTS: Our study shows that after a relatively short duration of ethanol ingestion, chickens developed LV dilatation and LV dysfunction. The serum concentrations of ethanol attained in this new model were similar to those reported in humans. Furthermore, unlike other currently available animal models of ethanol-induced cardiac disease, this model demonstrates myocyte hypertrophy, interstitial fibrosis, and myocytolysis, similar to observations in humanethanol-induced cardiac dysfunction. CONCLUSIONS: We conclude that this new avian model should provide a useful tool for investigating the mechanism(s) and pathophysiology of ethanol-induced dilated cardiomyopathy and heart failure.
Authors: Jennifer L Steiner; Anne M Pruznak; Maithili Navaratnarajah; Charles H Lang Journal: Alcohol Clin Exp Res Date: 2015-06-24 Impact factor: 3.455