Figure 1.

Amiodarone, but not sotalol, induced concentration-dependent impairment of mitochondrial respiration in intact platelets. (A) Representative trace of amiodarone-induced mitochondrial dysfunction (amiodarone-red; DMSO-grey). (B) Respiration of human platelets was measured after submaximal uncoupling with FCCP (2 µM). The concentration-dependent effect of amiodarone (red rhombus) and sotalol (green square) was measured by titrating increasing concentrations of each drug (15–240 µM) vs. the equivalent volume of vehicle (DMSO or H₂O). Non-mitochondrial respiration was evaluated by the inhibition of complex I with rotenone (2 µM) and complex III with antimycin A (1 µg/mL). (C) Representative trace of sotalol effect on mitochondrial respiration (sotalol-green; H₂O/solvent-grey). Data were expressed as mean ± SEM. Two-way ANOVA with Bonferroni post hoc test was performed on the antimycin-corrected data. ROX: residual oxygen consumption. DMSO: dimethyl sulfoxide. FCCP: carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone. ** p < 0.01 vs. DMSO. n = 5.