title: Reoxygenation-induced rigor-type contracture.
abstract: 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 micromol/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 micromol/l; (3) after 60-min anoxia Ca(20) was reduced to 0.78 +/- 0.05 micromol/l and (4) when energy recovery was accelerated (succinate, 0.2 mmol/l), Ca(20) rose to 1.35 +/- 0.05 micromol/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.
authors.affiliation: Physiologisches Institut, Justus-Liebig-Universität, Aulweg 129, Giessen D-35392, Germany.
authors.forename: Yury
authors.initials: Y
authors.lastname: Ladilov
authors.forename: Ozkan
authors.initials: O
authors.lastname: Efe
authors.forename: Claudia
authors.initials: C
authors.lastname: Schäfer
authors.forename: Bettina
authors.initials: B
authors.lastname: Rother
authors.forename: Sascha
authors.initials: S
authors.lastname: Kasseckert
authors.forename: Yaser
authors.initials: Y
authors.lastname: Abdallah
authors.forename: Karsten
authors.initials: K
authors.lastname: Meuter
authors.forename: Klaus
authors.initials: K
authors.lastname: Dieter Schlüter
authors.forename: Hans Michael
authors.initials: HM
authors.lastname: Piper
mesh_terms: D000818:Animals; D002118:Calcium / Q000032:analysis; D015687:Cell Hypoxia; D002478:Cells, Cultured; D003286:Contracture; D003600:Cytosol / Q000378:metabolism; D006352:Heart Ventricles / Q000166:cytology; D006863:Hydrogen-Ion Concentration; D008297:Male; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000378:metabolism*; D009206:Myocardium / Q000166:cytology; D032383:Myocytes, Cardiac / Q000166:cytology / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism* / Q000494:pharmacology; D010725:Phosphocreatine / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
chemical_list: D010725:Phosphocreatine; D010100:Oxygen; D002118:Calcium