A novel cardioprotective regimen for improvement of inner mitochondrial membrane function after ischemic stress.
Treatment of the normoxic working rat heart with 1 mmol/l 2-mercaptopropionylglycine (MPG) results in a significant increase of postischemic aortic flow. Measurement of N,N-dimethylaminostyrylmethylpyridinium iodide (DASPMI) fluorescence on the surface of the heart preparation gives semiquantitative information on mitochondrial energization in situ. No differences in fluorescence have been found between therapy and control groups. This finding is confirmed by fluorescence studies on isolated mitochondria. Investigations on postischemic mitochondrial oxygen consumption and ATPase clearly reveal ameliorated function of oxidative phosphorylation and reduced ATP splitting activity by MPG treatment. Mitochondrial energization (i.e. membrane potential) thus does not run strictly parallel with oxidative and phosphorylative capabilities.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000603:Amino Acids, Sulfur / Q000494:pharmacology*; D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000378:metabolism* / Q000517:prevention & control; D005260:Female; D066298:In Vitro Techniques; D007425:Intracellular Membranes / Q000378:metabolism*; D008929:Mitochondria, Heart / Q000378:metabolism*; D010085:Oxidative Phosphorylation / Q000187:drug effects; D010101:Oxygen Consumption; D051381:Rats; D011919:Rats, Inbred Strains; D013050:Spectrometry, Fluorescence; D008625:Tiopronin / Q000494:pharmacology*
D000603:Amino Acids, Sulfur; D008625:Tiopronin; D000251:Adenosine Triphosphatases