TITLE

Significant damage of the conduction system during cardioplegic arrest is due to necrosis not apoptosis

AUTHOR(S)
Sayk, Friedhelm; Krüger, Stefan; Bechtel, J.F. Matthias; Feller, Alfred C.; Sievers, Hans H.; Bartels, Claus
PUB. DATE
May 2004
SOURCE
European Journal of Cardio-Thoracic Surgery;May2004, Vol. 25 Issue 5, p801
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Objectives: Ventricular conduction disturbances following cardioplegic arrest remains a serious, yet unsolved problem. In the present study we examined whether myocardial conduction cells (MCC, Purkinje fibers) are more vulnerable to ischemia/reperfusion injury than working myocardial cells and whether the damage is due to necrosis or apoptosis. Methods: Mini-pigs were subjected to 60 min of crystalloid (St Thomas; n=15, group I) or blood (Buckberg; n=6, group II) cardioplegic arrest followed by 3 h of reperfusion. Animals not subjected to either procedures served as controls (n=5). Ventricular myocardial specimens were investigated by hematoxylin and eosin (HE) and periodic acid Schiff (PAS) staining and immunohistochemical labeling of apoptosis-associated proteins (Bax, Bcl-2, Caspase-3). DNA-breaks were visualized by in situ end labeling (terminal deoxynucleotidyl transferase dUTP-biotin nick-end labeling, TUNEL). Electron microscopy confirmed apoptosis or necrosis. Results: MCC of control hearts intrinsically expressed Bax, Bcl-2, and Caspase-3 without signs of either apoptotic or necrotic damage. Subendocardial Purkinje fibers of groups I and II hearts exhibited focal damage, with reduced labeling of apoptosis-associated proteins, glycogen loss, karyopycnosis and increased eosinophilia (15/21 hearts). The majority of damaged MCC displayed nuclear TUNEL-positivity (2.8±2.5% of MCC), whereas the average TUNEL-rate of the adjacent working myocardium was low (<0.1%). Electron microscopy demonstrated ischemic changes in MCC consistent with cellular necrosis. Conclusions: Ischemia/reperfusion injury due to cardioplegic arrest inflicts significant damage on subendocardial MCC, but not on working myocardium. Ultrastructural and light-microscopic findings are consistent with coagulation necrosis, rather than apoptosis.
ACCESSION #
12779354

 

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