Figure 5.

I/R in Langendorff-perfused mouse hearts ex vivo: CD39 inhibition enhances the overflow of renin and NE and prolongs arrhythmia (VT/VF) duration; these effects are prevented by selective blockade of P2X₇R. Coronary overflow of renin [angiotensin (ANG) I formed] and NE and duration of VT/VF in control ischemia (i.e., 40 min normothermic global ischemia), followed by 30 min reperfusion (n = 9). Other hearts were perfused with the CD39 inhibitor ARL67156 (30 µM; 10 min before ischemia and during the initial 15 min of reperfusion; n = 9), alone or together with the selective P2X₇R antagonist A740003 (3 µM; 5 min before ARL67156 and then together with it during the initial 15 min of reperfusion; n = 9). Bars represent means ± sem of renin; NE overflows during the first 5 min of reperfusion and duration of VT/VF measured during the entire 30 min of reperfusion. *P < 0.05 vs. I/R; ^#P < 0.05, ^##P < 0.01, and ^###P < 0.001 vs. I/R + ARL67156; ^†P < 0.05 vs. I/R by unpaired t-test, respectively.