Key result
Adolescent binge drinking in rats leads to ~2.5-fold more adult cardiac arrhythmias.
Why the study?
It was not well-known whether cardiovascular alterations elicited by adolescent binge drinking are reversible or persist into adulthood after long-term abstinence.
Does adolescent binge drinking induce long-lasting oxidative stress, inflammation, and cardiac dysfunction that persist into adulthood after long-term abstinence in Sprague-Dawley rats?
Does adolescent binge drinking induce long-lasting oxidative stress, inflammation, and cardiac dysfunction that persist into adulthood after long-term abstinence in Sprague-Dawley rats?
Absolute Event Rate: 53.6% vs 21.7%
p-value: p=<0.05
Adolescent binge drinking in rats induces persistent cardiac dysfunction, fibrosis, arrhythmogenesis, oxidative stress, and myocardial inflammation that remain present in early adulthood despite long-term abstinence.
Cardiovascular alterations from adolescent binge drinking may persist into adulthood despite abstinence; leaves open reversibility and antioxidant benefits in humans.
Background: It is not well-known whether cardiovascular alterations elicited by adolescent binge drinking (ABD) are reversible or if they persist following long-term abstinence until adult life. Thus, we studied the long-term impact of ABD on oxidative stress, inflammation and cardiovascular function. Methods: Twenty-four adolescent Sprague-Dawley rats underwent a controlled or ABD-like protocol, (ethanol 3.00 g/kg i.p.) starting at postnatal day 25 (PND25) to PND38, followed by long-term abstinence until PND70 (adulthood). Results: ABD resulted in overt cardiac dysfunction in adult rats. We found a decreased left ventricular compliance as evidenced by a marked reduction in the early-to-late mitral valve blood flow (E/A: 1.23 ± 0.14 vs. 1.51 ± 0.09, control vs. ABD, p < 0.05). Importantly, cardiac dysfunction was closely linked to adverse cardiac remodeling and fibrosis in ABD animals compared to control animals. Furthermore, we found that ABD resulted in a significant increase in cardiac arrhythmogenesis. Indeed, ABD rats showed a 2-fold increase in the incidence of cardiac arrhythmias compared to control rats (53.6 ± 12.7 vs. 21.7 ± 5.7 events/h, Control vs. ABD, p < 0.05). Finally, we found that cardiac functional impairments were accompanied by increases in cardiac tissue oxidative stress and upregulated levels of pro-inflammatory cytokines (i.e., IL-1β and TNF-α). Conclusions: Present results show that ABD drives long-lasting cardiac dysfunction that persists during early adulthood. Oxidative stress and inflammation may contribute to long-term cardiovascular alterations induced by ABD.
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Díaz et al. (2026) studied Adolescent binge drinking-induced cardiac dysfunction (n=24). Adolescent binge drinking-like protocol (ethanol) vs. Control protocol was evaluated on Left ventricular compliance (E/A ratio) and cardiac arrhythmia incidence (events/h) (p=<0.05). Adolescent binge drinking in rats reduced adult E/A ratio (1.23 vs 1.51, p<0.05) and doubled cardiac arrhythmias (53.6 vs 21.7 events/h, p<0.05) vs control.
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