The aim of the present study was to reveal by enzyme histochemistry and ultrastructural examination the possible anatomic substrate that may be the cause of high susceptibility of the pig heart to ischemia and/or reperfusion-induced severe arrhythmias. The heart of landrace pigs was subjected to 90 min of left coronary occlusion followed by 30 min reperfusion, whereby both conditions elicited arrhythmias and often even ventricular fibrillation. We found for the first time, besides common contractile cardiomyocytes, Purkinje fibers, and "transitional cells" in mid-myocardium. Transitional cells likely correspond to the recently described M cells. Importantly, these cells and Purkinje fibers exhibited reversible ischemia-related subcellular alterations, whereas the majority of contractile cardiomyocytes were irreversibly injured in the area of infarction. In correlation with these findings, glycogen-dependent phosphorylase activity was abolished, whereas it was still persistent in Purkinje fibers and small islands of contractile cardiomyocytes. Moreover, a distinct heterogeneity in the activity of all enzymes selected and subcellular alterations within a border zone were observed. These results suggest that particularly the preserved viability of specialized conducting cells spanning the ventricular wall may account for electrical disturbances that consequently contribute to increased susceptibility of the pig heart to ischemia- and reperfusion-induced severe arrhythmias.