Lisinopril alcohol
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Lisinopril and Alcohol: Interactions and Effects
Introduction to Lisinopril and Alcohol Interaction
Lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, is commonly prescribed for managing hypertension and heart failure. However, its interaction with alcohol, particularly chronic alcohol ingestion, has significant implications for various physiological systems, especially the cardiovascular and respiratory systems.
Oxidative Stress in the Lung
Alcohol-Induced Oxidative Stress
Chronic alcohol consumption is known to increase oxidative stress in the lungs, leading to conditions such as acute respiratory distress syndrome. This oxidative stress is characterized by increased superoxide production and elevated levels of NADPH oxidase subunits, such as gp91phox.
Role of Lisinopril in Mitigating Oxidative Stress
Lisinopril has been shown to attenuate the oxidative stress induced by chronic alcohol ingestion. In a study involving rats, lisinopril treatment reduced the levels of glutathione disulfide and superoxide formation in the lung parenchyma, which were elevated due to chronic alcohol consumption. This suggests that ACE inhibitors like lisinopril can play a protective role against alcohol-induced oxidative damage in the lungs.
Cardiovascular Implications
Alcohol and Myocardial Hypertrophy
Chronic alcohol ingestion can impair the regression of myocardial hypertrophy, even when treated with ACE inhibitors like lisinopril. In spontaneously hypertensive rats, alcohol consumption diminished the effectiveness of lisinopril in reducing left ventricular mass and contractile protein levels. This indicates that alcohol can interfere with the therapeutic effects of lisinopril on the heart, potentially complicating the management of hypertensive patients who consume alcohol.
Protein Metabolism and Enzyme Activity
The study also found that alcohol ingestion altered protein metabolism and enzyme activities in the heart. While lisinopril increased the activities of proteases such as cathepsin D and dipeptidyl aminopeptidase I in control rats, these effects were not observed in alcohol-consuming rats. This further underscores the negative impact of alcohol on the efficacy of lisinopril in treating hypertrophic myocardium.
Pulmonary Barrier Dysfunction
Alcohol and Epithelial Barrier Dysfunction
Alcohol abuse can lead to significant pulmonary complications, including epithelial barrier dysfunction and increased expression of transforming growth factor-beta1 (TGF-beta1). This dysfunction is exacerbated during conditions like sepsis, leading to severe lung injury.
Protective Role of Lisinopril
Lisinopril has been found to mitigate these adverse effects by normalizing glutathione levels and reducing TGF-beta1 expression. In ethanol-fed rats, lisinopril treatment improved alveolar epithelial barrier function and limited TGF-beta1 protein release into the alveolar space during endotoxemia. This highlights the potential of lisinopril in protecting the lungs from alcohol-induced damage.
Conclusion
The interaction between lisinopril and alcohol presents a complex scenario where chronic alcohol ingestion can significantly impair the therapeutic effects of lisinopril, particularly in the cardiovascular and respiratory systems. While lisinopril shows promise in mitigating oxidative stress and pulmonary barrier dysfunction induced by alcohol, its efficacy in reducing myocardial hypertrophy is compromised in the presence of alcohol. These findings underscore the importance of considering alcohol consumption in patients undergoing treatment with ACE inhibitors like lisinopril.
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