Reperfusion Injury Induces Apoptosis in Rabbit Cardiomyocytes

Reperfusion Injury Induces Apoptosis in Rabbit Cardiomyocytes

Volume 94, October 1994, 1621–1628 | Roberta A. Gottlieb, Katharine O. Burleson, Robert A. Kloner, Bernard M. Babior, and Robert L. Engler
The study investigates the role of apoptosis in reperfusion injury in rabbit cardiomyocytes. Apoptosis, a form of programmed cell death, is characterized by the formation of nucleosomal DNA fragments (≈ 200 base pairs). The researchers found that nucleosomal ladders of DNA fragments were detected in ischemic/reperfused rabbit myocardial tissue but not in normal or ischemic-only hearts. This indicates that apoptosis is a specific feature of reperfusion injury, leading to late cell death. The study also explored the contribution of granulocytes and used in situ nick end labeling to identify the cell type undergoing apoptosis. Electron microscopy revealed distinct patterns of nuclear chromatin condensation in reperfused and persistently ischemic tissue, suggesting that reperfusion-specific injury processes occur. The findings suggest that reperfusion injury can be distinguished from ischemic injury, which has implications for understanding and potentially preventing late cell death in cardiac myocytes.The study investigates the role of apoptosis in reperfusion injury in rabbit cardiomyocytes. Apoptosis, a form of programmed cell death, is characterized by the formation of nucleosomal DNA fragments (≈ 200 base pairs). The researchers found that nucleosomal ladders of DNA fragments were detected in ischemic/reperfused rabbit myocardial tissue but not in normal or ischemic-only hearts. This indicates that apoptosis is a specific feature of reperfusion injury, leading to late cell death. The study also explored the contribution of granulocytes and used in situ nick end labeling to identify the cell type undergoing apoptosis. Electron microscopy revealed distinct patterns of nuclear chromatin condensation in reperfused and persistently ischemic tissue, suggesting that reperfusion-specific injury processes occur. The findings suggest that reperfusion injury can be distinguished from ischemic injury, which has implications for understanding and potentially preventing late cell death in cardiac myocytes.
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