REPERFUSION INJURY INDUCES APOPTOSIS IN RABBIT CARDIOMYOCYTES

The most effective way to limit myocardial ischemic necrosis is reperf usion, but reperfusion itself may result in tissue injury, which has b een difficult to separate from ischemic injury. This report identifies elements of apoptosis (programmed cell death) in myocytes as a respon se to reperfusion but not ischemia. The hallmark of apoptosis, nucleos omal ladders of DNA fragments (approximate to 200 base pairs), was det ected in ischemic/reperfused rabbit myocardial tissue but not in norma l or ischemic-only rabbit hearts. Granulocytopenia did not prevent nuc leosomal DNA cleavage. In situ nick end labeling demonstrated DNA frag mentation predominantly in myocytes. The pattern of nuclear chromatin condensation was distinctly different in reperfused than in persistent ly ischemic tissue by transmission electron microscopy. Apoptosis may be a specific feature of reperfusion injury in cardiac myocytes, leadi ng to late cell death.