Journal
CIRCULATION RESEARCH
Volume 104, Issue 1, Pages 15-U35Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCRESAHA.108.186429
Keywords
cardioprotection; infarct size; reperfusion injury
Funding
- German Research Foundation [SK182/1-1]
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Ischemic postconditioning (IPoC) reduces infarct size following ischemia/reperfusion. Whether or not phosphorylation of RISK (reperfusion injury salvage kinases) (AKT, ERK1/2, P70S6K, GSK3 beta) is causal for protection by IPoC is controversial. We therefore studied the impact of RISK on IPoC in anesthetized pigs subjected to 90 minutes of left anterior descending coronary artery hypoperfusion and 120 minutes of reperfusion. In protocol 1, IPoC, by 6 cycles of 20/20 seconds of reperfusion/reocclusion (n = 13), was compared with immediate full reperfusion (IFR) (n = 15). In protocol 2, IPoC (n = 4) or IFR (n = 4) was performed with pharmacological RISK blockade by IC coinfusion of Wortmannin and U0126. Infarct size was determined by TTC staining, and the expression of phosphorylated RISK proteins by Western blot analysis in biopsies. In protocol 1, infarct size was 20 +/- 3% (percentage of area at risk; mean +/- SEM) with IPoC and 33 +/- 4% (P< 0.05) with IFR. RISK phosphorylation increased with reperfusion but was not different between IPoC and IFR. In protocol 2, Wortmannin and U0126 blocked the increases in RISK phosphorylation during reperfusion, but infarct size was still smaller with IPoC (15 +/- 7%) than with IFR (35 +/- 6%; P< 0.05).
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