Functional behaviour of isolated heart muscle mitochondria after in situ ischemia. Polarographic analysis of mitochondrial oxidative phosphorylation.
Heart muscle mitochondria with satisfactory functional parameters of oxidative phosphorylation and with morphologically intact structure were isolated from canine myocardium employing a modified KEA-medium (0.18 M KCl, 10 mM EDTA, 0.5% bovine serum albumin, pH 7.1) according to Sordahl and Schwartz (1). The functional behaviour of mitochondria was investigated after different durations of in situ ischemia (cardioplegia, 15 degrees C) and correlated with metabolic findings. During ischemia the following changes were seen: 1. Successive reduction of electron flow. 2. Relatively small impairment of phosphorylation efficiency. 3. Less damage of FAD- than NAD-catalyzed oxidative phosphorylation. 4. A marked increase of electron flow and thus recovery of phosphorylation rate even after longer ischemic periods by addition of cytochrome c. As important factors of accelerating mitochondrial impairment during ischemia the myocardial ATP decrease, the lactate and H+-activity increase are discussed.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003326:Coronary Circulation; D003327:Coronary Disease / Q000378:metabolism*; D003574:Cytochrome c Group / Q000494:pharmacology; D004285:Dogs; D006324:Heart Arrest, Induced; D007773:Lactates / Q000378:metabolism; D008854:Microscopy, Electron; D008929:Mitochondria, Heart / Q000378:metabolism*; D009206:Myocardium / Q000473:pathology; D010085:Oxidative Phosphorylation; D011048:Polarography
D003574:Cytochrome c Group; D007773:Lactates; D000255:Adenosine Triphosphate