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Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
Published on: April 17, 2021
Ischemic postconditioning in pigs: no causal role for RISK activation
Andreas Skyschally1, Patrick van Caster, Kerstin Boengler
1Institut für Pathophysiologie, Universitätsklinikum Essen, Germany.
Circulation Research
|November 29, 2008
Summary
Ischemic postconditioning (IPoC) significantly reduces heart attack size in pigs. However, RISK pathway activation is not essential for this protective effect, suggesting other mechanisms are involved.
Area of Science:
- Cardiovascular Science
- Myocardial Infarction Research
- Cellular Signaling
Background:
- Ischemic postconditioning (IPoC) is a protective strategy against ischemia/reperfusion injury.
- The role of reperfusion injury salvage kinases (RISK) pathway phosphorylation in IPoC's efficacy remains debated.
Purpose of the Study:
- To investigate the causal role of RISK pathway phosphorylation in the infarct-limiting effects of IPoC.
- To determine if RISK pathway activation is necessary for IPoC-induced cardioprotection.
Main Methods:
- Anesthetized pigs underwent 90 minutes of coronary artery hypoperfusion followed by 120 minutes of reperfusion.
- IPoC was induced using cycles of reperfusion/reocclusion, compared to immediate full reperfusion (IFR).
- RISK pathway blockade was achieved using Wortmannin and U0126, with infarct size assessed by TTC staining and protein phosphorylation by Western blot.
Main Results:
- IPoC reduced infarct size (20% vs. 33% of area at risk) compared to IFR.
- RISK pathway phosphorylation increased with reperfusion but showed no significant difference between IPoC and IFR groups.
- Pharmacological blockade of RISK pathways abolished phosphorylation increases but did not negate IPoC's infarct-reducing effect (15% vs. 35% of area at risk).
Conclusions:
- RISK pathway phosphorylation is not essential for the infarct-reducing benefits of ischemic postconditioning.
- These findings suggest that IPoC-mediated cardioprotection involves mechanisms independent of RISK pathway activation.
