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| This article is part of the supplement: 3rd International Symposium on the Pathophysiology of Cardiopulmonary Bypass. Myocardial cell damage and myocardial protectionMeeting abstractInduction of myocardial heat shock protein-60 after cardioplegic arrest and reperfusionDepartment of Cardiac Surgery, University of Ulm, Ulm, Germany Aachen, Germany. 16 December 2000 Critical Care 2001, 5(Suppl B):P2doi:10.1186/cc995
© 2001 BioMed Central Ltd IntroductionCardiomyocytes 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. MethodFrom 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. ResultsIn 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. ConclusionWe 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. Have something to say? Post a comment on this article! |



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