Reoxygenation-induced rigor-type contracture

The hypothesis tested was that reoxygenation-induced contracture of myocardial cells, a form of reperfusion injury, can be due to a rigor-type mechanism. Isolated adult cardiomyocytes were exposed to 30- or 60-min anoxia (pH 6.4) and reoxygenation (pH 7.4). In cardiomyocytes, cytosolic Ca2+ and cell length, and in isolated rat hearts left ventricular end-diastolic pressure (LVEDP) were measured. During reoxygenation, cardiomyocytes developed contracture. When energy recovery was slowed down, less Ca2+ overload was required for contracture: (1) after 30-min anoxia Ca20 (cytosolic Ca2+ concentration in cells with 20% cell length reduction) was 1.42 ± 0.11 μmol/l; (2) after 30-min anoxia with partial mitochondrial inhibition during reoxygenation (NaCN, 0.1 mmol/l) Ca20 was reduced to 0.69 ± 0.05 μmol/l; (3) after 60-min anoxia Ca20 was reduced to 0.78 ± 0.05 μmol/l and (4) when energy recovery was accelerated (succinate, 0.2 mmol/l), Ca20 rose to 1.35 ± 0.05 μmol/l. In isolated hearts, the reperfusion-induced rise in LVEDP was modulated by the same interventions. Slow recovery of energy production favors reoxygenation-induced contracture in cardiomyocytes and hearts. This shows that rigor contracture contributes to reoxygenation-induced cell injury.