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Preoperative glucocorticoids decrease pulmonary hypertension in piglets after cardiopulmonary bypass and circulatory

Jeffrey M Pearl1, Steven M Schwartz, David P Nelson

  • 1Department of Cardiology, Cincinnati Children's Hospital Medical Center, OH, USA. jeffrey.pearl@cchmc.org

The Annals of Thoracic Surgery
|March 3, 2004
PubMed
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Glucocorticoids, specifically methylprednisolone, prevent pulmonary hypertension after cardiopulmonary bypass and deep hypothermic circulatory arrest. This protective effect is linked to reduced endothelin-1 and nuclear factor-kappaB activation.

Area of Science:

  • Cardiovascular Surgery
  • Pediatric Cardiology
  • Pharmacology

Background:

  • Glucocorticoids are routinely used in pediatric patients undergoing congenital heart defect repair with cardiopulmonary bypass.
  • The precise mechanisms by which glucocorticoids improve cardiopulmonary recovery after cardiopulmonary bypass and deep hypothermic circulatory arrest remain incompletely understood.

Purpose of the Study:

  • To investigate the hypothesis that glucocorticoids can enhance cardiopulmonary recovery following cardiopulmonary bypass and deep hypothermic circulatory arrest.
  • To elucidate the underlying mechanisms of glucocorticoid action in this context.

Main Methods:

  • Crossbred piglets underwent deep hypothermic circulatory arrest (120 minutes) during cardiopulmonary bypass.
  • Methylprednisolone was administered either intraoperatively or preoperatively and intraoperatively.

Related Experiment Videos

  • Control animals received saline without glucocorticoids.

    • Main Results:

    • Preoperative and intraoperative glucocorticoid administration prevented the increase in pulmonary vascular resistance observed in controls.
    • Glucocorticoid treatment significantly reduced plasma endothelin-1 levels post-procedure.
    • Reduced pulmonary intercellular adhesion molecule-1 and myeloperoxidase activity were noted in glucocorticoid-treated groups.
    • Increased inhibitor kappaBalpha levels indicated nuclear factor-kappaB pathway inhibition.

    Conclusions:

    • Glucocorticoids effectively prevent pulmonary hypertension after cardiopulmonary bypass and deep hypothermic circulatory arrest.
    • Reduced endothelin-1, intercellular adhesion molecule-1, and myeloperoxidase activity contribute to the protective effects of glucocorticoids.
    • Inhibition of nuclear factor-kappaB and decreased neutrophil activation are key mechanisms underlying glucocorticoid-induced cardiopulmonary protection.