Anti‐arrhythmic effect of remote ischemic preconditioning is accompanied by changes in the salvage kinases in the rat heart non‐ischemic area

Abstract

Remote ischemic preconditioning (RIPC) by intermittent ligation and reperfusion of femoral arteries decreases the occurrence and the duration of reperfusion arrhythmias. We sought to study whether salvage kinases (RISK) are involved in this phenomenon. Rats in the RIPC group were subjected to 3 cycles of bilateral femoral artery occlusion + reperfusion (5 min each) followed by 5 min of coronary artery occlusion with subsequent 1 min of reperfusion. In the ischemia/reperfusion (IR) group femoral arteries were exposed but not ligated. After a 30 min waiting period coronary artery was occluded and reperfused as in the RIPC group. At the end of the reperfusion the risk area was delineated with blue dye and hearts were frozen in liquid nitrogen. Non‐ischemic (NI) and ischemic (Isc) areas were separated and Western blots were performed for phospho‐Akt (p‐Akt) and phospho‐p70S6 (p‐p70S6). In the NI area the levels of kinases were reduced in the RIPC vs. IR group by 55% and 58% for p‐Akt and p‐p70S6 respectively (p<0.05). In the Isc vs. NI area of both groups kinases were equally increased and reached levels of ~2.7 baseline‐normalized units. The Isc/NI ratio in the RIPC vs. IR group was increased by 131% and 154% for p‐Akt and p‐p70S6 respectively (p<0.05). Our data suggest that RIPC increased parameters of RISK in the ischemic area to equivalent of IR alone, but reduced these parameters in the NI zone to a greater extent than IR.