Abstract
Introduction: Binge alcohol drinking adversely impacts cardiovascular (CV) homeostasis, leading to increased risk of CV diseases. It is also well-established that chronic alcohol consumption causes gut dysbiosis. However, the effects of alcohol-induced gut dysbiosis on vascular endothelial function remains unknown. Methods: We studied C57BL/6 mice at 10 weeks of age for these studies with n = 8-18 mice per group. Mice underwent a binge-on-chronic alcohol (BoCA) feeding protocol for 20-days and received either vehicle or probiotic treatment. Aortic vascular reactivity (acetylcholine and sodium nitroprusside), plasma nitrite (HPLC) and 8-isoprostane levels (ELISA) were measured. Another group of mice (n = 11-12 per group) received broad-spectrum antibiotic treatments followed by gut microbiotic transplants from either pair-fed or BoCA fed donor mice and plasma nitrite levels were measured to assess vascular function. Results: BoCA resulted in impaired endothelium-dependent vascular relaxation which was accompanied by reduced plasma nitrite levels. Probiotic treatment significantly attenuated vascular dysfunction, increased plasma nitrite and reduced 8-isoprostane levels. Further, mice receiving gut microbiotic transfer from alcohol-treated donor mice exhibited reduced circulating nitrite levels when compared to those who receiving the transfer from pair-fed donor mice. Conclusions: Our data demonstrate that BoCA consumption induced vascular injury resulting in reduced NO bioavailability, impaired vascular relaxation, and elevated oxidative stress which was attenuated by probiotic treatment. Mice receiving gut microbiotic contents from BoCA fed donor mice displayed reduced NO bioavailability, suggesting that gut dysbiosis is involved in the detrimental cardiovascular effects of BoCA. Further studies are underway to define the mechanisms by which alcohol-induced gut dysbiosis promotes cardiovascular disease.
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