[Factor released during myocardial ischemia reperfusion may become a marker of opening of the mitochondrial permeability transition pore].
In experiments on isolated hearts of guinea-pigs, on a model of ischemia-reperfusion cardiac reperfusion has been shown to result in a constriction of coronary vessels, arrhythmia, an inhibition of the contractile activity of the myocardium, and an increase in an oxygen cost of the myocardial work. Apart from that, a stable agent was detected in a reperfusion solution by spectrophotometry on the wave length of 250 nM. Similar deterioration of the heart function and the availability of the stable agent in the solution were observed under influence of the known activators of mitochondrial permeability transition pore-phenilarsine oxide and antimycin A. In anaesthetized animals a release of the stable factor into the blood was induced by either ischemia-reperfusion or those activators. Application of the known inhibitors of the mitochondrial permeability transition pore cyclosporin A or trolox (water-soluble vitamin E) decreased remarkably both the cardiodynamic deterioration and a release of the stable factor under heart reperfusion. Mitochondrial origin of the factor was confirmed in experiments on isolated mitochondria. Thus, the detected factor has been determined to be released from mitochondria at the opening of mitochondrial permeability transition pore and is thought to be the marker of its opening in experiments in vitro and in vivo.
D000818:Animals; D015415:Biomarkers / Q000032:analysis; D006168:Guinea Pigs; D066298:In Vitro Techniques; D015640:Ion Channel Gating / Q000502:physiology*; D007473:Ion Channels / Q000378:metabolism*; D008565:Membrane Proteins / Q000032:analysis / Q000096:biosynthesis*; D008929:Mitochondria, Heart / Q000378:metabolism*; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D009200:Myocardial Contraction / Q000502:physiology; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology; D013053:Spectrophotometry; D016277:Ventricular Function, Left / Q000502:physiology
D015415:Biomarkers; D007473:Ion Channels; D008565:Membrane Proteins; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore