Mitochondrial damage during myocardial ischemia |
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Authors: | V Regitz D J Paulson R J Hodach S E Little W Schaper A L Shug PhD |
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Institution: | (1) Departments of Neurology and Physiology, University of Wisconsin-Madison and William S. Middleton Memorial Veterans Hospital Madison, Wisconsin;(2) Max-Planck-Institut für experimentelle Kardiologie, Bad Nauheim, FRG;(3) Present address: Metabolic Research Lab., Wm. S. Middleton Memorial VA Hospital, 2500 Overlook Terrace, 53705 Madison, Wisconsin |
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Abstract: | Summary The effects of 3 hours of ischemia and 1 hour of reperfusion on biochemical, physiological and ultrastructural parameters were studied in 12 dogs. In the ischemic subendocardium without reperfusion, mitochondrial losses of adenine (ATP+ADP+AMP) and pyridine (NAD+NADH) nucleotides far exceeded those observed in whole tissue. Adenine nucleotide translocator (aNT) was severely inhibited and seemed to, be a sensitive indicator of a lesion of the inner mitochondrial membrane.Postischemic reperfusion led to a slight loss of adenine and pyridine nucleotides from the reversibly damaged subepicardium and to an enorous loss from the irreversibly damaged subendocardium. The washout of nucleotides from irreversibly damaged areas caused the negative para-Nitro Blue Tetrazolium (pNBT) staining of the infarcted tissue. Diagnosis of cell death with pNBT failed after the occlusion period without reflow because pyridine, although lost from the mitochondria, was still present in the tissue. In reversibly injured areas, mitochondrial function and ultrastructure were restored after reperfusion, although a significant nucleotide loss was found in the tissue. These studies suggest that mitochondrial ultrastructure and function may play a key role in cellular viability during recovery from ischemia.Supported by NIH Grant HL 17736 and the Veterans Administration, and the Max-Planck-Institut für experimentelle Kardiologie |
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Keywords: | ischemia reperfusion adenine pyridine mitochondria |
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