Key result
Ischemic preconditioning reduces infarct size ~52% versus control, but translational blockade reverses this protection.
Why the study?
Does protein synthesis inhibition abolish the cardioprotective effects of ischemic or pharmacological preconditioning in isolated rabbit hearts?
Does protein synthesis inhibition abolish the cardioprotective effects of ischemic or pharmacological preconditioning in isolated rabbit hearts?
Absolute Event Rate: 22% vs 46%
p-value: p=<0.01
Protein synthesis at the translational level is required for the cardioprotective effects of ischemic preconditioning, but not pharmacological preconditioning with pinacidil.
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Translational dependence distinguishes IPC from pinacidil protection in rabbit hearts; leaves open mechanistic translation to clinical cardioprotection.
Matsuyama et al. (2000) studied Ischemia/reperfusion injury. Ischemic preconditioning (IPC) and pharmacological preconditioning (pinacidil) vs. Control (no treatment) was evaluated on Infarct size as a percentage of the area at risk (p=<0.01). Ischemic preconditioning and pinacidil reduced infarct size compared with control (22% and 27% vs 46%, P<0.01), but translational blockade with cycloheximide reversed the protective effect of IPC.
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