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Attenuated cardioprotection by ischemic preconditioning in coronary stenosed heart and its restoration by carvedilol

Kenichi Watanabe1, Hiroyuki Yaoita, Kazuei Ogawa

  • 1First Department of Internal Medicine, Fukushima Medical University, Hikarigaoka 1, Fukushima 960-1295, Japan.

Cardiovascular Research
|June 20, 2006
PubMed

Insights

Ischemic preconditioning (IPC) reduces infarct size (IS), but this effect is weakened in hearts with chronic coronary stenosis (CS). Carvedilol treatment restored this protective mechanism in a rat model.

Area of Science:

  • Cardiovascular Research
  • Ischemic Heart Disease
  • Pharmacology

Background:

  • Ischemic preconditioning (IPC) is a phenomenon that reduces infarct size (IS) in the heart.
  • The efficacy of IPC in the context of chronic coronary stenosis (CS)-induced ischemia is not well understood.
  • Understanding how CS affects IPC is crucial for developing effective therapeutic strategies.

Purpose of the Study:

  • To investigate the impact of chronic coronary stenosis (CS) on infarct size (IS) reduction by ischemic preconditioning (IPC).
  • To explore the role of the mitochondrial KATP channel (mitoKATP) and protein kinase C (PKC)-epsilon in mediating IPC effects under CS.
  • To evaluate the potential of carvedilol as a therapeutic agent to restore cardioprotection in CS-induced ischemic hearts.

Main Methods:

  • Assessed IS in rat hearts with CS (1-12 weeks) subjected to acute coronary occlusion and reperfusion.
  • Evaluated modifications in IS by IPC, mitoKATP opener/blocker, and daily carvedilol treatment.
  • Measured myocardial PKC-epsilon activity in risk areas using Western blotting.

Main Results:

  • CS-induced PKC-epsilon activation was observed early after CS but attenuated later.
  • IPC and mitoKATP opener-mediated IS reduction were diminished at later time points post-CS.
  • Daily carvedilol treatment restored PKC-mitoKATP signaling and the cardioprotective effects of IPC and mitoKATP opener.

Conclusions:

  • Chronic coronary stenosis (CS) initially activates cardioprotective PKC-mitoKATP signaling, mimicking IPC.
  • This protective effect is downregulated late after CS, leading to attenuated IPC efficacy.
  • Carvedilol may offer novel cardioprotection in CS-induced ischemic hearts by restoring this signaling pathway.
Abstract

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