A comparative study on ischaemia- or anoxia-induced impairment of myocytic structure and cardiac function in the isolated, isovolumicly-contracting, perfused rat heart

Impairment of contractile function and extent of release of several intracellular marker enzymes and DNA were studied in isolated perfused rat hearts after low-flow (0.16 ml·min−1) ischaemia followed by 2 h of reperfusion and after anoxia followed by 2 h of reoxygenation. After varying periods of ischaemia or anoxia, the hearts were analysed for cytoplasmic, lysosomal and mitochondrial enzymes, for nuclear DNA and for increase in heart weight (oedema formation). Recovery of contractile function, weight increase and release of lactate dehydrogenase (LDH), a cytoplasmic enzyme, were measured as a function of duration of ischaemia or anoxia. Myocardial enzyme activities and DNA content after varying periods of ischaemia or anoxia were compared with myocardial LDH activity. The study demonstrates that the ultimate extent of enzyme depletion after ischaemia + reperfusion differs significantly from that after anoxia + reoxygenation in respect of mitochondrial enzymes. For mitochondrial aspartate aminotransferase and monoamine oxidase ultimate depletion is 64 ± 8% and 114 ± 22%, respectively, for hearts after ischaemia + reperfusion, and 7 ± 8% and 58 ± 11%, respectively, for hearts after anoxia + reoxygenation. It is concluded that mitochondrial damage, as reflected by mitochondrial enzyme release from the heart, is less marked after anoxia + reoxygenation than after ischaemia + reperfusion at corresponding extent of LDH depletion.