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Lethal myocardial ischemic injury

R B Jennings, K A Reimer

    The American Journal of Pathology
    |February 1, 1981
    PubMed
    Summary
    This summary is machine-generated.

    Severe ischemia in myocytes causes high-energy phosphate depletion and membrane damage, marking irreversible injury. While similar in vitro and in vivo, in vitro models offer clearer insights into cell death mechanisms during myocardial ischemia.

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    Area of Science:

    • Cardiovascular Biology
    • Cellular Physiology
    • Biochemistry

    Background:

    • Myocardial ischemia leads to cellular injury, progressing from reversible to irreversible stages.
    • Understanding the biochemical and structural changes in ischemic myocytes is crucial for identifying cell death mechanisms.

    Purpose of the Study:

    • To review the biologic changes in severely ischemic myocytes, focusing on high-energy phosphate metabolism, adenine nucleotide pool destruction, and sarcolemma damage.
    • To compare ischemic events in vivo with those in vitro to identify potential lethal cellular events.

    Main Methods:

    • Estimation of high-energy phosphate (HEP) production via anaerobic glycolysis by measuring lactate accumulation.
    • Estimation of total HEP utilization by measuring the depletion of preformed HEP stores.

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  • Assessment of ultrastructural and functional evidence of sarcolemma disruption in irreversibly injured tissue.
  • Main Results:

    • Between 80-90% of HEP utilized by ischemic dog left ventricle is produced by anaerobic glycolysis.
    • Irreversibility onset correlates with marked depletion of HEP and adenine nucleotide pools, and cessation of glycolysis.
    • Irreversibly injured tissue shows ultrastructural and functional disruption of the sarcolemma.

    Conclusions:

    • Severe high-energy phosphate depletion and sarcolemma damage are objective signs of irreversible myocardial ischemic injury.
    • Events in severe in vivo ischemia are similar to in vitro ischemia but occur more slowly in vitro.
    • The causal relationship between HEP depletion, membrane damage, and cell death in ischemia remains unproven.