<p><b>A</b>, MitoPY1 fluorescence (535 nm) in control (black) and IP (grey) in Langendorff-perfused hearts subjected to 30 min ischemia + 30 min reperfusion. Fluorescence was normalized to the 1 min pre-iscaemic value. MitoPY1 was successfully loaded into the hearts as shown by the increase in fluorescence upon addition of H<sub>2</sub>O<sub>2</sub> to the perfusion medium. <b>B,</b> Mean 535 nm fluorescence (± SEM as error bars) was normalized to the average value between 20.5 and 21.5 min obtained on reperfusion after 30 min global ischemia in control (black, n = 10) and IP hearts (grey, n = 8). <b>C</b>, Corresponding autofluorescence data for hearts subject to a mock loading protocol (n = 6 in both control and IP hearts). Corresponding infarct sizes are presented in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0167300#pone.0167300.t001" target="_blank">Table 1</a>. <b>D</b>, Aconitase activity in mitochondria isolated from normoxic control hearts (Cont) and both control (CP Rep) and ischemic preconditioned (IP Rep) hearts subjected to 30 min ischemia and 90 s reperfusion as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0167300#pone.0167300.s001" target="_blank">S1 Fig</a> The grey bars confirm the reduction in aconitase activity following treatment of the mitochondrial extract with 200 μmol/L H<sub>2</sub>O<sub>2</sub>. Data are given as means ± SEM (error bars) of 4 hearts in each group.</p
