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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 79 (1984), S. 207-217 
    ISSN: 1435-1803
    Keywords: ischemia ; reperfusion ; adenine ; pyridine ; mitochondria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 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.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-1803
    Keywords: Malondialdehyde ; thiobarbituric-acid-reactive material ; reactiveoxygen species ; isolatedrat heart ; reperfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We tested the effect of exogenous purine derived free radicals and H2O2 VS ischemia and reperfusion on the thiobarbituric-acid (TBA)-reactive material and malondialdehyde (MDA) formation in isolated rat hearts using the thiobarbituric acid test and high performance lipid chromatography (HPLC). We could not detect increased thiobarbituric-acid-reactive material or MDA- production during 6 MM H2O2 infusion, during free radical generation by purine-derived free radicals, or using ischemia and reperfusion. Increased thiobarbituric-acid-reactive material and MDA tissue levels were detected only during infusion of 12 mM H2O2 (p〈0.001). We conclude that the generally used thiobarbituric acid assay for MDA is susceptible to artifacts and unsuited as an indirect measure for low-to-medium-levels of oxygen free radicals. Using HPLC assay, which accurately measures MDA, no evidence was found that MDA is a primary and direct lipid peroxidation product of exogenous or endogenous reactive oxygen species.
    Type of Medium: Electronic Resource
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