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

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• 作者：Sayk ; Friedhelm ; Krü ; ger ; Stefan ; Bechtel ; J.F. Matthias ; Feller ; Alfred C. ; Sievers ; Hans H. ; et. al.
• 关键词：Purkinje fibers ; Conduction system ; Cardioplegia ; Apoptosis ; Oncosis ; Necrosis
• 刊名：European Journal of Cardio-Thoracic Surgery
• 出版年：2004
• 出版时间：May, 2004
• 年：2004
• 卷：25
• 期：5
• 页码：801-806
• 全文大小：436 K

文摘

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.