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Volume 5 Supplement 7

3rd International Symposium on the Pathophysiology of Cardiopulmonary Bypass. Myocardial cell damage and myocardial protection

Induction of myocardial heat shock protein-60 after cardioplegic arrest and reperfusion


Cardiomyocytes respond to stress with the expression of various heat shock proteins (HSPs). Expression of mitochondrial HSP60 is known to be induced by various stress factors, including ischaemia and reperfusion. The aim of the study was to investigate the induction of HSP60 in human myocardium during cardiac surgery.


From eight patients undergoing elective coronary artery bypass grafting or valve replacement, samples of right atrium were harvested before and after extracorporeal circulation (ECC). Two patients had atrial fibrillation and six were in sinus rhythm. The myocardial samples were excised and immediately immersed in liquid nitrogen. The HSP60 protein level was determined using sodium dodecyl sulphate-polyacrylamide gel electrophoresis, Western blot, and subsequent ECL technique. The amount of HSP60 protein was quantified by optical densitometry, according to the immunoreactive bands of actin.


In all samples HSP60 was detected before and after ECC. We could not find any difference in HSP60 expression before and during cardiac surgery. There was no correlation with duration of cardiopulmonary bypass or reperfusion time.


We could not demonstrate a cytoprotective upregulation of HSP60 after an obligatory period of ischaemia, cardioplegic arrest and reperfusion. This might reflect effective cardioprotection during ECC.

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Schäfler, A., Kirmanoglou, K., Scheunert, T. et al. Induction of myocardial heat shock protein-60 after cardioplegic arrest and reperfusion. Crit Care 5, P2 (2001).

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  • Heat Shock
  • Coronary Artery Bypass Grafting
  • Valve Replacement
  • HSP60 Expression
  • HSP60 Protein