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Related Experiment Videos

Failure to precondition pathological human myocardium.

S Ghosh1, N B Standen, M Galiñianes

  • 1Department of Surgery, University Hospitals Leicester, United Kingdom.

Journal of the American College of Cardiology
|November 6, 2001
PubMed
Summary
This summary is machine-generated.

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Ischemic preconditioning protects the heart, but this effect is lost in diabetic patients due to mitochondrial KATP channel dysfunction. This dysfunction in diabetic hearts involves signal transduction pathways distinct from these channels.

Area of Science:

  • Cardiology
  • Mitochondrial Physiology
  • Diabetic Cardiomyopathy

Background:

  • Conflicting evidence exists regarding ischemic preconditioning (PC) as a phenomenon in healthy hearts.
  • The efficacy of PC in diseased myocardium, particularly in diabetic and failing hearts, remains unclear.

Purpose of the Study:

  • To investigate the effects of ischemic preconditioning (PC) on diabetic and failing human myocardium.
  • To determine the role of mitochondrial KATP channels in the response to PC in these diseased tissues.

Main Methods:

  • Human atrial appendages from seven groups (nondiabetic, diabetic types, varying ejection fractions) were used.
  • Muscle slices underwent aerobic control, ischemia-alone, PC, diazoxide (Mito KATP opener), or glibenclamide (KATP blocker) treatments.

Related Experiment Videos

  • Creatine kinase leakage and MTT reduction were assessed to measure injury and cell viability.

    • Main Results:

    • Ischemia induced similar injury in normal and diseased tissues.
    • PC protected against ischemia in all groups except noninsulin-dependent diabetics (NIDD), insulin-dependent diabetics (IDD), and hearts with ejection fraction <30%.
    • Diazoxide mimicked protection in most groups, but not in NIDD or IDD. Glibenclamide abolished protection in nondiabetic and diet-controlled NIDD groups.

    Conclusions:

    • Failure of PC in diabetic hearts is attributed to mitochondrial KATP channel dysfunction.
    • The mechanism of PC failure in diabetic hearts involves signal transduction pathways separate from mitochondrial KATP channels.