Key result
Intermittent cross-clamp fibrillation improved recovery of function compared to control (61% vs 41%, p<0.05), an effect attenuated by protein kinase C inhibition or K(ATP)-channel blockade.
Why the study?
Does intermittent cross-clamp fibrillation improve recovery of function and reduce myocardial injury in isolated Langendorff-perfused rat hearts via an ischemic preconditioning mechanism?
Population
Isolated Langendorff-perfused rat hearts
Comparison
Intermittent cross-clamp fibrillation (with or… vs Control group
Design
Preclinical
Follow-up
60 min (reperfusion)
Authors
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Supports PKC- and K(ATP)-mediated preconditioning in rat hearts; leaves open translation to clinical myocardial protection.
Does intermittent cross-clamp fibrillation improve recovery of function and reduce myocardial injury in isolated Langendorff-perfused rat hearts via an ischemic preconditioning mechanism?
Absolute Event Rate: 61% vs 41%
p-value: p=<0.05
Cardioprotection induced by intermittent cross-clamp fibrillation in isolated rat hearts is mediated by ischemic preconditioning mechanisms involving protein kinase C and mitochondrial K(ATP) channels.
Fujii et al. (2005) studied Myocardial ischemia/reperfusion injury. Intermittent cross-clamp fibrillation vs. Control (ischemia) or pharmacological blockade was evaluated on Recovery of function (left ventricular developed pressure) (p=<0.05). Intermittent cross-clamp fibrillation improved recovery of function compared to control (61% vs 41%, p<0.05), an effect attenuated by protein kinase C inhibition or K(ATP)-channel blockade.
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