Abstract
Alcohol abuse causes 79,000 deaths stemming from severe organ damage in the United States every year. Clinical manifestations of long-term alcohol abuse on the cardiac muscle include defective contractility with the development of dilated cardiomyopathy and low-output heart failure; which has poor prognosis with less than 25% survival for more than three years. In contrast, low alcohol consumption has been associated with reduced risk of cardiovascular disease, however the mechanism of this phenomenon remains elusive. The aim of this study was to determine the significance of apoptosis as a mediating factor in cardiac function following chronic high alcohol versus low alcohol exposure. Adult rats were provided 5 mM (low alcohol), 100 mM (high alcohol) or pair-fed non-alcohol controls for 4–5 months. The hearts were dissected, sectioned and stained with cresyl violet or immunohistochemically for caspase-3, a putative marker for apoptosis. Cardiomyocytes were isolated to determine the effects of alcohol exposure on cell contraction and relaxation. High alcohol animals displayed a marked thinning of the left ventricular wall combined with elevated caspase-3 activity and decreased contractility. In contrast, low alcohol was associated with increased contractility and decreased apoptosis suggesting an overall protective mechanism induced by low levels of alcohol exposure.
Highlights
Alcohol abuse is one of the most relevant and disabling issues that plagues our society
Gross histological observations suggest a thinning of the left ventricular wall of high-alcohol subjects compared to both control and low-alcohol subjects (Figure 1)
We set out to ascertain the levels of positive caspase-3 events in the hearts of rats exposed to high alcohol, low alcohol, and no alcohol by performing an immunohistochemical and cardiomyocyte contractility analysis
Summary
Alcohol abuse is one of the most relevant and disabling issues that plagues our society. It is the third leading preventable cause of death in the United States with an average of 79,000 casualties every year [1]. Results from the National Epidemiological Survey on Alcohol and Related Conditions performed in 2001–2002 show that 30.3% of adults in the United States have experienced alcohol use disorders at some point during their lives [2]. A major contributor of health-care expenses related to excess alcohol consumption is asymptomatic alcoholic cardiomyopathy (ACM) [3] which can lead to progressive heart failure with or without reduced ventricular wall thickness and cardiac output, accompanied with electrocardiogram (ECG) abnormalities [3,4]. Apoptosis is a regulated process of cell deletion that is characterized by events that result in nuclear and cellular fragmentation, as well as cell shrinkage [6]
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