Apoptosis in the conduction system of the heart in the senscence accelerated mouse (SAM)

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*Background and Purpose* Cardiac disorders such as heart block often develop in aged patients, but the pathogenesis remains unexplained. The senescence accelerated mouse (SAM) is a novel murine model of accelerated senescence. To clarify loss of cardiocytes in the conduction system of aging heart, atrioventricular (AV) conducting tissue from SAM was examined with conventional light (LM) and transmission electron microscopy (EM). Both of light ane electron microscopic in situnick end labeling of dUTP (TUNEL) was also applied. *Results* LM showed atrophic myocardial cells with shrunk nuclei occasionally but not very often. EM revealed that cardiocytes sporadically underwent a variety of degenerative processes, which were characterized by disorganization of myofibrils and intermediate filaments, enlarged sarcoplasmic reticulum, intracytoplasmic vacuoles, curvilinear membranous formation, and rare disruptions of the plasma membrane. Nuclear chromatin was condensed and marginated beneath apparently preserved nuclear membrane in some degenerated cardiocytes. In the interstitium, some macrophages appeared to have phagocytosed degenerated cardiocytes and included some residual bodies, but there was no infiltration of inflammatory cells. Cardiocytes degenerated more often in AV conducting tissue than in working myocardium. Furthermore, light and electron microscopic TUNEL-positive cardiocytes were seen occasionally in AV conducting tissu. *Conclusion* It is concluded that myocardial cell death in AV conduction system of SAM hearts may be induced by apoptosis which is programd in aging process of conducting cardiocytes.