Abstract 163: Protective Effects of L-Carnitine on Left Ventricular and Myocyte Dysfunction after Short-Term Oral Alcohol Administration in Rat
Background. Recent observations indicate that alcohol exposure induces cardiac injury through the induction of oxidative stress. L-carnitine (LC), a natural-occurring amino acid and an essential cofactor, has a well-known antioxidant action. LC increases the clearance of ethanol from the blood. Thus, we tested the hypothesis that LC therapy may limit or prevent alcohol-induced cardiac dysfunction after short-term oral ethanol administration.
Method. We measured alcohol-intake caused changes of left ventricular (LV) tissue levels of malonyldial-dehyde (MDA) and assessed LV and myocyte functional performance and myocyte [Ca2+]i transient ([Ca2+]iT) response in 3 groups of male adult SD rats (BW, 300 to 350g) over 8–10 days: 12 rats received 20% alcohol (2 g/kg administered intragastrically, once per day in the early morning); 12 received alcohol and LC (LC 50 mg/kg administered daily i.p., 60 min before alcohol intake); and 10 were controls.
Results. Compared with controls, alcohol ingestion caused significant increase in cardiac MDA (27%, 5.10 vs 4.02 μg/g wet weight of LV) followed by decreased LV contractility (EES: 0.55 vs 0.92 mmHg/μl; MSW: 56.6 vs 85.9 mmHg), ejection fraction (EF, 30 vs 52%) and increased the time constant of LV relaxation (τ, 14.4 vs 11.9 ms). These changes were paralleled with significant reductions in myocyte systolic amplitude (SA, 7.4 vs 10.4%), the peak velocity of shortening (dL/dtmax, 104.3 vs 160.8 μm/s), and peak systolic [Ca2+]iT (0.18 vs 0.25) (p<0.05). Treatment with LC prevented alcohol-induced decreases in LV contractility (EES, 0.97 mmHg/μl; MSW: 81.2 mmHg), EF (51%) and an increase in τ (12.7 ms). Myocyte contraction measured as SA (10.3%), dL/dtmax (151.3 μm/s), and [Ca2+]iT (0.22) were close to control values.
Conclusions. In rats, short-term alcohol consumption induces myocardial oxidative stress and depresses LV and myocyte contractile performance and [Ca2+]iT. Supplementation with LC prevents alcohol-induced LV and myocyte dysfunction. These findings may support the usefulness of LC as a potential therapeutic agent in alcohol abusers.