[Studies on the mechanism of arrhythmogenic action of free fatty acid].

It was reported that free fatty acid (FFA) is one of the important factors which cause ventricular arrhythmias during acute myocardial infarction. However the mechanism is still unclear. Measuring ventricular fibrillation threshold (VFT), the mechanism of FFA was investigated in perfused rat heart. The perfusion of 0.12 mM albumin alone, 0.12 mM palmitate bound to 0.12 mM albumin and 0.36 mM palmitate bound to 0.12 mM albumin didn't lower VFT significantly. However 0.60 mM palmitate bound to 0.12 mM albumin lowered VFT from 2.19 +/- 0.20 mA to 1.56 +/- 0.13 mA. The perfusion of 0.36 mM palmitate bound to 0.12 mM fatty acid binding protein (FABP) lowered VFT from 2.05 +/- 0.19 mA to 1.47 +/- 0.23 mA, but 0.12 mM FABP alone didn't. The perfusion of 0.36 mM palmitate bound to 0.12 mM FABP caused VFT to fall greater than 0.36 mM palmitate bound to 0.12 mM albumin perfusion, though the difference was not statistically significant. The VFT fall induced by the perfusion of 0.60 mM palmitate bound to 0.12 mM albumin was suppressed by 0.1 microM Verapamil perfusion and reduction of perfusate Ca2+ concentration from 2.5 mM to 1.67 mM. These results suggest that FFA lowered VFT by increasing the uptake into the cells due to carrier proteins such as FABP and that FFA-induced VFT fall was suppressed by reduction of Ca2+ entry into the cells.