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Related Experiment Videos

Characterization of postischemic myocardial oxygen utilization.

I B Krukenkamp, N A Silverman, D Sorlie

    Circulation
    |November 1, 1986
    PubMed
    Summary

    This study found that myocardial oxygen consumption (MVO2) increases after cardioplegic arrest, indicating improved heart function. This elevated MVO2 serves as a reliable marker for cardioplegic efficacy, independent of other factors.

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    Area of Science:

    • Cardiology
    • Physiology
    • Biochemistry

    Background:

    • Potassium-induced arrest is used in cardiac procedures.
    • Previous studies noted perturbations in myocardial oxygen consumption (MVO2) after such arrests.

    Purpose of the Study:

    • To define the perturbations in myocardial oxygen consumption (MVO2) after potassium-induced arrest.
    • To investigate MVO2 as a potential marker for cardioplegic efficacy.

    Main Methods:

    • MVO2 was measured in 19 canine hearts during isovolumetric pressure-volume loading.
    • Measurements were taken before and after 2 hours of cardioplegic ischemia at 20°C.
    • The effects of propranolol were assessed post-ischemia.

    Main Results:

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  • Postischemic MVO2, indexed per beat and per left ventricular weight, was augmented by 40% (p < .05).
  • This increased oxygen utilization persisted despite coronary hyperemia attenuation, normalized oxygen extraction, and beta-adrenergic blockade.
  • Propranolol depressed peak developed pressure and heart rate post-ischemia.

    • Conclusions:

    • Increased MVO2 to generate physiologic pressures is a sensitive biological marker for cardioplegic efficacy.
    • This marker is independent of coronary flow and oxygen uptake.
    • The increased MVO2 is not solely due to increased beta-adrenergic stimulation.