抄録
Background: Increasing alcohol intake is known to link to increased risk of atrial fibrillation that has possibly been associated with apoptosis. Recent studies have revealed that ethanol induces apoptosis of various tissues. However, apoptotic effects of ethanol on atrium are unclear. Therefore, we hypothesized that ethanol induces apoptosis of atrium, and prove the hypothesis using HL-1 mouse atrial myocytes. Methods and Results: The cultured HL-1 cells were incubated for 18 hours with 0.25, 0.50, 1.0, and 2.0% of ethanol. To determine apoptosis in HL-1 cells, mitochondrial transmembrane potential (ΔΨm), the percentage of the cells with hypodiploid DNA, and the activity of caspase-3 were measured quantitatively by flow cytometric assay with DiOC6(3), propidium iodide, and PhiPhiLux G1D2, respectively. Ethanol at 1.0% or more induced loss of ΔΨm, the occurrence of hypodiploid cells, and activation of caspase-3. Conclusions: Ethanol induced apoptosis of HL-1 cells, suggesting that ethanol intake leads to structural remodeling of atrial myocytes through the induction of apoptosis, followed by the development of the arrhythmogenic substrate, which tends to initiate and perpetuate atrial fibrillation. [J Physiol Sci. 2007;57 Suppl:S207]
