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1 Cardiology, Aarhus University Hospital, Skejby, Aarhus N, Aarhus, Denmark; , Rosenvangs Alle 232, Hoejbjerg, Aarhus, DK-8270, Denmark
2 Cardiac Surgery, Aarhus University Hospital, Skejby, Aarhus N, Aarhus, Denmark
3 Cardiovascular Surgery, Hospital for Sick Children, Toronto, Canada
4 Cardiology, Hospital for Sick Children Toronto, Toronto, Canada
5 Cardiology, Royal Children's Hospital, Australia
6 Papworth Hospital, United Kingdom
7 Department of Cardiology, Aarhus University Hospital, Skejby Sygehus, Aarhus N, Denmark
8 Cardiology, Aarhus University Hospital, Skejby, Aarhus N, Aarhus, Denmark
9 Toronto General Hostal, Toronto, Canada
10 Cardiology, University of Toronto, Toronto, Canada
11 Department of Medicine, University of Cambridge, United Kingdom
* To whom correspondence should be addressed. E-mail: andrew.redington{at}sickkids.ca.
Background: Remote ischemic preconditioning reduces myocardial infarction (MI) in animal models. We tested the hypothesis that the systemic protection thus induced is effective when administered during ischemia and prior to reperfusion, and examined the role of the K-ATP channel. Methods and results: Twenty 20-kg pigs were randomized (10 in each group) to a 40-minute period of left anterior descending artery occlusion with 120-minutes reperfusion. Remote perconditioning (PerC) was four 5-minute cycles of lower limb ischemia by tourniquet, during LAD occlusion. Left ventricular (LV) function was assessed using a conductance catheter and extent of infarction by tetrazolium staining. The extent of myocardial infarction was significantly reduced by PerC (60.4±14.3% vs. 38.3±15.4%, p=0.004). This was associated with improved functional indices: The increase in time constant of diastolic relaxation (
) was significantly attenuated by PerC compared to control in both ischemia and reperfusion phases (p=0.01, p=0.04 respectively). At 120-minutes reperfusion there was a 38±6% in control reduction in preload recruitable stroke work versus 3±5% in the PerC group (p=0.001). The force-frequency relationship was significantly depressed at 120-minutes reperfusion in both groups, but the optimal heart rate was significantly lower in the control group (p=0.04). Furthermore, there were fewer malignant arrhythmias with PerC during reperfusion (p=0.02). These protective effects of PerC were abolished by glibenclamide. Conclusion: Intermittent limb ischemia during myocardial ischemia reduces myocardial infarction, preserves global systolic and diastolic function, and protects against arrhythmia during the reperfusion phase through a K-ATP dependent mechanism. Understanding this process may have important therapeutic implications for a range of ischemia-reperfusion syndromes.
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