Reoxygenation-induced rigor-type contracture

• Published in: Journal of molecular and cellular cardiology Vol. 35; no. 12; pp. 1481 - 1490
• Main Authors: Ladilov, Yury, Efe, Özkan, Schäfer, Claudia, Rother, Bettina, Kasseckert, Sascha, Abdallah, Yaser, Meuter, Karsten, Dieter Schlüter, Klaus, Piper, Hans Michael
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.12.2003
• Subjects: Animals; Ca 2; Calcium - analysis; Cell Hypoxia; Cells, Cultured; Contracture; Cytosol - metabolism; Energy metabolism; Heart Ventricles - cytology; Hydrogen-Ion Concentration; Male; Myocardial Ischemia - metabolism; Myocardial Ischemia - physiopathology; Myocardial Reperfusion Injury - metabolism; Myocardium - cytology; Myocytes; Myocytes, Cardiac - cytology; Myocytes, Cardiac - metabolism; Oxygen - metabolism; Oxygen - pharmacology; Phosphocreatine - analysis; Rats; Rats, Wistar; Reperfusion; Time Factors; Energy metabolism; Reperfusion; Myocytes; Ca 2
• ISSN: 0022-2828; 1095-8584
• DOI: 10.1016/j.yjmcc.2003.09.016

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 Ca 2+ 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 Ca 2+ overload was required for contracture: (1) after 30-min anoxia Ca 20 (cytosolic Ca 2+ 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) Ca 20 was reduced to 0.69 ± 0.05 μmol/l; (3) after 60-min anoxia Ca 20 was reduced to 0.78 ± 0.05 μmol/l and (4) when energy recovery was accelerated (succinate, 0.2 mmol/l), Ca 20 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.