INTRODUCTION: The effect of remote ischemic preconditioning (RIPC) on arrhythmias in in vivo models is unknown. Our purpose was to determine effects of both acute and delayed RIPC on arrhythmias. METHODS AND RESULTS: In the acute protocol anesthetized open chest rats were exposed to 5 minutes of proximal left coronary artery occlusion (CAO) and 10 minutes of reperfusion. Rats were either untreated (ischemia/reperfusion, IR group, n = 17) or received RIPC (n = 14) with 5 minutes bilateral femoral occlusions followed by 5 minutes of reperfusion times 3, started 30 minutes before CAO. At reperfusion, onset of ventricular tachycardia (VT) was delayed in RIPC group (25.7 seconds) versus IR (8.8 seconds; P = 0.04). Number of episodes of VT was 17.0 in IR versus 3.0 in the RIPC group (P = 0.01) and duration of VT was 54.1 seconds in IR versus 4.9 seconds in RIPC (P = 0.019). Number of ventricular premature complexes (VPC) was 26.0 in IR and 10.0 in RIPC rats (P = 0.04). Levels of reperfusion injury salvage kinases (RISK), that is, phospho-Akt and phospho-p70S6 in the risk area of IR and RIPC hearts were similarly higher compared to the nonischemic areas both at 1 and 10 minutes into reperfusion. Delayed RIPC was induced on day 1 and on day 2, myocardial IR was induced. Delayed RIPC did not affect VT or VPC. CONCLUSION: Acute RIPC of the lower limbs induced a powerful delay in/and reduction in IR induced ventricular arrhythmias, but without evoking the RISK pathway; a late protective phase of RIPC on arrhythmias did not occur.
INTRODUCTION: The effect of remote ischemic preconditioning (RIPC) on arrhythmias in in vivo models is unknown. Our purpose was to determine effects of both acute and delayed RIPC on arrhythmias. METHODS AND RESULTS: In the acute protocol anesthetized open chest rats were exposed to 5 minutes of proximal left coronary artery occlusion (CAO) and 10 minutes of reperfusion. Rats were either untreated (ischemia/reperfusion, IR group, n = 17) or received RIPC (n = 14) with 5 minutes bilateral femoral occlusions followed by 5 minutes of reperfusion times 3, started 30 minutes before CAO. At reperfusion, onset of ventricular tachycardia (VT) was delayed in RIPC group (25.7 seconds) versus IR (8.8 seconds; P = 0.04). Number of episodes of VT was 17.0 in IR versus 3.0 in the RIPC group (P = 0.01) and duration of VT was 54.1 seconds in IR versus 4.9 seconds in RIPC (P = 0.019). Number of ventricular premature complexes (VPC) was 26.0 in IR and 10.0 in RIPCrats (P = 0.04). Levels of reperfusion injury salvage kinases (RISK), that is, phospho-Akt and phospho-p70S6 in the risk area of IR and RIPC hearts were similarly higher compared to the nonischemic areas both at 1 and 10 minutes into reperfusion. Delayed RIPC was induced on day 1 and on day 2, myocardial IR was induced. Delayed RIPC did not affect VT or VPC. CONCLUSION: Acute RIPC of the lower limbs induced a powerful delay in/and reduction in IR induced ventricular arrhythmias, but without evoking the RISK pathway; a late protective phase of RIPC on arrhythmias did not occur.
Authors: Michael M Galagudza; Dmitry L Sonin; Timur D Vlasov; Dmitry I Kurapeev; Eugene V Shlyakhto Journal: Int J Exp Pathol Date: 2016-03-18 Impact factor: 1.925
Authors: Amir S Lotfi; Hossein Eftekhari; Auras R Atreya; Ananth Kashikar; Senthil K Sivalingam; Miguel Giannoni; Paul Visintainer; Daniel Engelman Journal: World J Cardiol Date: 2016-10-26