Mitochondrial membrane potentials in ischemic hearts

• Published in: Archives of biochemistry and biophysics 2003-12, Vol.420 (2), p.279-286
• Main Authors: Berkich, Deborah A, Salama, Guy, LaNoue, Kathryn F
• Format: Article
• Language: English
• Subjects: Animals; Blood Pressure - drug effects; Blood Pressure - physiology; Calcium - metabolism; Cell Membrane Permeability - physiology; Cyclosporin A; Cyclosporine - pharmacology; Electrophysiology - methods; Heart; Intracellular Membranes - physiology; Ischemia; Male; Membrane Potentials - physiology; Mitochondria, Heart - physiology; Mitochondrial membrane potential; Mitochondrial permeability transition; Myocardial Ischemia - physiopathology; Myocardial Reperfusion Injury - physiopathology; Onium Compounds - chemistry; Onium Compounds - metabolism; Organophosphorus Compounds - chemistry; Organophosphorus Compounds - metabolism; Phosphocreatine - metabolism; Rats; Rats, Sprague-Dawley; Tritium
• ISSN: 0003-9861; 1096-0384
• DOI: 10.1016/j.abb.2003.09.021

Excised rat hearts were perfused isovolumically and then made globally ischemic for times varying from 0 to 70 min followed by 50 min of reperfusion. In situ mitochondrial electrical potential gradients (Δ ψ m) were measured during reperfusion using the lipophilic cation, 3H-tetraphenylphosphonium. Therefore, it was possible to measure the relationships between mechanical performance, Δ ψ m, and high energy phosphates as a function of time of ischemia. The absolute value of Δ ψ m remained constant and then dropped sharply in parallel with mechanical performance after 35 min of ischemia. Eliminating Ca 2+ from the reperfusate medium did not preserve Δ ψ m nor increase high energy phosphates during the recovery period. An inhibitor of the mitochondrial permeability transition, cyclosporin A, delayed the fall in Δ ψ m but did not eliminate it. The data suggest that the mitochondrial permeability transition plays a role in ischemic cell death but is not triggered by influx of Ca 2+ through the plasma membrane.