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Related Experiment Videos

Ischemic preconditioning targets the reperfusion phase.

Derek J Hausenloy1, Abigail M Wynne, Derek M Yellon

  • 1The Hatter Cardiovascular Institute, University College London Hospital and Medical School, 67 Chenies Mews, London, WC1E 6HX, UK.

Basic Research in Cardiology
|May 29, 2007
PubMed
Summary
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Ischemic preconditioning (IPC) protection requires protein kinase C (PKC) activation, mitochondrial ATP-sensitive potassium (mKATP) channel opening, redox signaling, and acidosis during reperfusion. These factors are essential for reducing infarct size after heart ischemia.

Area of Science:

  • Cardiology
  • Physiology
  • Biochemistry

Background:

  • Emerging research indicates that signaling events during myocardial reperfusion play a role in ischemic preconditioning (IPC).
  • The specific requirement of protein kinase C (PKC) activation, mKATP channel opening, redox signaling, and transient acidosis during reperfusion for IPC-induced cardioprotection remains unclear.

Purpose of the Study:

  • To investigate whether PKC activation, mKATP channel opening, redox signaling, and transient acidosis during myocardial reperfusion are necessary for mediating the protective effects of IPC.

Main Methods:

  • Langendorff-perfused rat hearts underwent 35 minutes of ischemia followed by 120 minutes of reperfusion.
  • Infarct size was determined using tetrazolium staining.
  • Hearts were treated during the initial 15 minutes of reperfusion with either a vehicle control (DMSO), a PKC antagonist (chelerythrine), an mKATP channel blocker (5-hydroxydecanoate), an ROS scavenger (N-mercaptopropionylglycine), or a buffer to counteract acidosis (NaHCO3).

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Main Results:

  • All four tested agents (chelerythrine, 5-hydroxydecanoate, N-mercaptopropionylglycine, and NaHCO3) administered during reperfusion abolished the infarct size reduction typically observed with IPC.
  • Vehicle control hearts showed a 49.3% infarct size, reduced to 21.0% with IPC (P<0.05).
  • In contrast, hearts treated with inhibitors or scavengers during reperfusion showed no significant difference in infarct size between control and IPC groups, indicating a loss of IPC's protective effect.

Conclusions:

  • This study provides the first evidence that protein kinase C (PKC) activation, opening of the mitochondrial ATP-sensitive potassium (mKATP) channel, redox signaling, and transient acidosis occurring specifically during the myocardial reperfusion phase are critical for mediating the cardioprotective effects of ischemic preconditioning (IPC).