Reperfusion injury induces apoptosis in rabbit cardiomyocytes. This study identifies apoptosis as a response to reperfusion but not ischemia. Apoptosis, characterized by nucleosomal DNA fragmentation (200 base pairs), was detected in ischemic/reperfused rabbit myocardial tissue but not in normal or ischemic-only hearts. Granulocytopenia did not prevent nucleosomal DNA cleavage. In situ nick end labeling showed DNA fragmentation predominantly in myocytes. Transmission electron microscopy revealed distinct nuclear chromatin condensation patterns in reperfused versus persistently ischemic tissue. Apoptosis may be a specific feature of reperfusion injury in cardiac myocytes, leading to late cell death. The study used an animal model with New Zealand white rabbits, inducing ischemia and reperfusion, and analyzing DNA fragmentation and electron microscopy. Apoptosis was confirmed in reperfused tissue but not in ischemic-only tissue. Granulocytopenic animals showed similar apoptosis patterns, indicating that cell types other than PMNs undergo apoptosis. In situ nick end labeling identified myocytes as the primary source of nucleosomal DNA fragmentation. Electron microscopy showed distinct nuclear chromatin patterns in reperfused tissue, suggesting reperfusion-specific injury. The study highlights the role of apoptosis in reperfusion injury and its potential as a target for therapeutic intervention.Reperfusion injury induces apoptosis in rabbit cardiomyocytes. This study identifies apoptosis as a response to reperfusion but not ischemia. Apoptosis, characterized by nucleosomal DNA fragmentation (200 base pairs), was detected in ischemic/reperfused rabbit myocardial tissue but not in normal or ischemic-only hearts. Granulocytopenia did not prevent nucleosomal DNA cleavage. In situ nick end labeling showed DNA fragmentation predominantly in myocytes. Transmission electron microscopy revealed distinct nuclear chromatin condensation patterns in reperfused versus persistently ischemic tissue. Apoptosis may be a specific feature of reperfusion injury in cardiac myocytes, leading to late cell death. The study used an animal model with New Zealand white rabbits, inducing ischemia and reperfusion, and analyzing DNA fragmentation and electron microscopy. Apoptosis was confirmed in reperfused tissue but not in ischemic-only tissue. Granulocytopenic animals showed similar apoptosis patterns, indicating that cell types other than PMNs undergo apoptosis. In situ nick end labeling identified myocytes as the primary source of nucleosomal DNA fragmentation. Electron microscopy showed distinct nuclear chromatin patterns in reperfused tissue, suggesting reperfusion-specific injury. The study highlights the role of apoptosis in reperfusion injury and its potential as a target for therapeutic intervention.