Glucocorticoids improve calcium cycling in cardiac myocytes after cardiopulmonary bypass

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Jeffrey M Pearl1, David M Plank, Kelly M McLean

  • 1Division of Cardiothoracic Surgery, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.

The Journal of Surgical Research
|September 4, 2009
PubMed

Insights

Glucocorticoids preserve cardiac function after cardiopulmonary bypass by maintaining myocyte calcium cycling and reducing calpain activation. This study shows methylprednisolone therapy improves heart function post-CPB.

Area of Science:

  • Cardiology
  • Biochemistry
  • Physiology

Background:

  • Cardiopulmonary bypass (CPB) can lead to myocardial dysfunction due to ischemia and reperfusion injury.
  • Glucocorticoids are known to mitigate this dysfunction.
  • The study investigates if methylprednisolone preserves cardiac function post-CPB by maintaining myocyte calcium cycling.

Purpose of the Study:

  • To test the hypothesis that methylprednisolone therapy preserves cardiac function after CPB by maintaining myocyte calcium cycling.
  • To evaluate the effect of methylprednisolone on calcium handling in cardiac myocytes post-CPB.
  • To assess the impact of methylprednisolone on specific molecular markers related to cardiac function and injury.

Main Methods:

  • Piglets underwent CPB with or without methylprednisolone (CPB-GC or CPB). Control (No-CPB) piglets did not undergo CPB.
  • Myocardial function was assessed in vivo, and calcium cycling was analyzed in isolated cardiac myocytes using confocal microscopy.
  • Molecular analyses included phospholamban phosphorylation, SERCA2a protein levels, and calpain activation in myocardial tissue.

Main Results:

  • Methylprednisolone (CPB-GC) maintained preload recruitable stroke work post-CPB, unlike in the CPB group.
  • In myocytes, methylprednisolone prevented the prolongation of calcium transient time and blunting of amplitude observed in the CPB group.
  • Glucocorticoid treatment reduced calpain activation and maintained phospholamban phosphorylation and SERCA2a protein levels compared to CPB alone.

Conclusions:

  • Glucocorticoid-mediated improvement in myocardial function post-CPB is partly due to the prevention of calpain activation.
  • Methylprednisolone therapy helps maintain cardiac myocyte calcium cycling, thereby preserving cardiac function after CPB.
  • These findings highlight the role of calcium handling and calpain activity in CPB-induced myocardial dysfunction.
Abstract

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