ALCOHOL-INDUCED CARDIOTOXICITY: EXPLORING THE IMPACT ON BLOOD VESSELS AND HEART FUNCTION

Abstract

This study investigates the effects of chronic alcohol consumption on heart function and vascular health, specifically focusing on alcohol-induced cardiotoxicity. Using a rodent model, rats were exposed to ethanol (20% v/v) for 12 weeks, and various cardiovascular, biochemical, and molecular parameters were assessed. Histological analysis revealed significant myocardial remodeling, including increased fibrosis and hypertrophy in the alcohol-treated group compared to controls. Functional assessments indicated elevated systolic and diastolic blood pressure, along with a reduced heart rate in alcohol-treated rats, suggesting compromised cardiac function and autonomic regulation. The Examined samples displayed elevated MDA levels and reduced SOD and GPX levels indicating increased oxidative stress through biochemical evaluations. The alcohol-exposed group displayed increased expression of pro-inflammatory cytokines TNF-α and IL-6 together with pro-apoptotic BAX and decreased BCL-2 expression which indicates inflammatory and apoptotic reactions occur within the myocardium. Other research studies demonstrate that heart tissue exposure to alcohol connects to oxidative damage, inflammation and structural modifications. Analysis demonstrates that long-term alcohol use creates major cardiovascular abnormalities which produce heart tissue alterations and vascular system breakdown and causes imbalanced inflammatory and oxidative mechanisms. Additional research must pursue specific treatment approaches which handle alcohol-related cardiovascular damage since oxidative stress and inflammation play essential roles in developing alcohol-induced heart disease. Further investigation needs to explore interventions against alcohol-induced adverse effects and genetic factors which affect vulnerability to alcohol-related cardiotoxicity.