Postconditioning: A Form of “Modified Reperfusion” Protects the Myocardium by Activating the Phosphatidylinositol 3-Kinase-Akt Pathway
Why the study?
Does ischemic postconditioning reduce infarct size and activate the PI3K-Akt pathway in isolated perfused rat hearts subjected to ischemia and reperfusion?
Population
Isolated perfused rat hearts subjected to 35 minutes of ischemia
Comparison
Ischemic postconditioning vs Standard reperfusion without postconditioning…
Design
Preclinical
Follow-up
120 minutes or 7 minutes of reperfusion
Authors
Discussion
Loading...
Member takes
Implication
Does not inform clinical reperfusion strategies; extends PI3K-Akt mediation evidence in rat postconditioning models.
Structured PICO
Does ischemic postconditioning reduce infarct size and activate the PI3K-Akt pathway in isolated perfused rat hearts subjected to ischemia and reperfusion?
P
Population
Isolated perfused rat hearts subjected to 35 minutes of ischemia
I
Intervention
Ischemic postconditioning (brief intermittent episodes of ischemia and reperfusion at the onset of reperfusion)
C
Comparator
Standard reperfusion without postconditioning, or postconditioning with PI3K inhibitors (LY or Wortmannin)
O
Outcome
Infarct size (determined by tetrazolium staining) and phosphorylation states of Akt, eNOS, and p70S6Ksurrogate
Ischemic postconditioning protects the myocardium against reperfusion injury by activating the prosurvival kinases PI3K-Akt, eNOS, and p70S6K.
Cite This Study
Tsang et al. (2004) studied this question.