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Related Experiment Videos

Mechanisms underlying myocardial stunning

W Flameng1

  • 1Department of Cardiac Surgery, Centre of Experimental Surgery and Anaesthesiology, Katholieke Universiteit Leuven, Belgium.

Journal of Cardiac Surgery
|March 1, 1993
PubMed
Summary
This summary is machine-generated.

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Myocardial stunning impairs sarcoplasmic reticulum (SR) calcium uptake velocity during ischemia, but this recovers upon reperfusion. This suggests SR dysfunction, beyond Ca2+ ATPase, contributes to stunning and altered heart contractions.

Area of Science:

  • Cardiology
  • Cardiovascular Physiology
  • Mitochondrial Function

Background:

  • Myocardial stunning is a post-ischemic dysfunction.
  • Previous studies indicated preserved mitochondrial high-energy phosphate content after ischemia and reperfusion.
  • The role of excitation-contraction coupling alterations in myocardial stunning requires further investigation.

Purpose of the Study:

  • To examine the effect of myocardial stunning on sarcoplasmic reticulum (SR) function.
  • To investigate the impact of ischemia and reperfusion on SR calcium uptake and release.
  • To determine the contribution of SR dysfunction to altered cardiac contractility during stunning.

Main Methods:

  • Rabbit hearts subjected to global normothermic ischemia followed by reperfusion.

Related Experiment Videos

  • Measurement of SR calcium (Ca2+) uptake velocity (Vmax).
  • Assessment of myocardial ATP content.
  • Evaluation of potentiated contractions, including post-rest potentiation (PRP) and peak paired-pulse potentiation (PPP), using a Langendorff heart model.

    • Main Results:

    • Ischemic hearts showed significantly reduced SR Ca2+ uptake velocity (Vmax) and myocardial ATP content compared to controls.
    • SR Ca2+ uptake velocity and ATP content returned to normal levels upon reperfusion.
    • Ryanodine incubation did not affect the differences in Vmax, suggesting SR Ca2+ pumping, not release, was affected.
    • Ischemia led to increased PRP and PPP, with further increases in PPP but a decrease in PRP of left ventricular pressure and dP/dt upon reperfusion.

    Conclusions:

    • Myocardial stunning involves impaired SR Ca2+ uptake velocity during ischemia, which is reversible upon reperfusion.
    • SR Ca2+ ATPase function is unlikely to be the primary cause of myocardial stunning.
    • Alterations in SR function, distinct from Ca2+ ATPase, contribute to the impaired excitation-contraction coupling and altered contractility observed in myocardial stunning.