Figure 3. Modulation of mK_ATP activity and IPC-mediated cardioprotection by fluoxetine.

(A): FLX dose-response of mK_ATP activity. Activity was measured using the BTC-AM-Tl⁺ assay. Data were plotted as % mK_ATP inhibition, with 100% inhibition defined as the condition in the presence of 1 mmol/L ATP, and 0% closed (i.e. open) being the baseline (Ctrl.) condition without ATP. FLX experiments were measured in the absence of ATP. Curve fit using the Hill equation revealed the FLX IC₅₀ to be 2.39 ± 0.22 μmol/L. Data are means ± SEM, N≥4. (B): mK_ATP activity was measured by the BTC-AM-Tl⁺ assay. Where indicated, FLX or ZM were present. Data are means ± SEM, N≥4. *P<0.05 versus control. (C): Effect of FLX or ZM on IR injury and IPC. Hearts were subjected to Langendorff perfusion as detailed in the methods. Infarct size / area at risk was quantified from TTC staining, with representative stained hearts shown above each condition. Data are means ± SEM, N≥4, *P<0.05 vs. IR. (D): Rate pressure product (RPP, expressed as % of initial) in hearts subjected to each protocol. Data are split across two panels for clarity (IR data shown in both panels), and are means ± SEM, N≥4. *P<0.05 vs. IR, ^#P<0.05 vs. IPC+IR. The initial RPP (mmHg·min⁻¹, ×10³) for each group is listed in the legend.