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  • 1
    ISSN: 1435-1803
    Keywords: heart ; dog ; oxygen deficiency ; adenine metabolites ; electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a previous study we found that the development of fine structural alteration in atrial myocardium made ischaemicin vivo was slower than has been observed for ventricular myocardium. To explore possible reasons for this, parallel samples of atrial (A) and ventricular (V) myocardium undergoing autolysis (ischaemic necrosis)in vitro at 37°C were studied for up to 2 hours. At 15-minute intervals tissue was snap-frozen for measurement of pH, lactate, and adenine metabolites by HPLC. In half the experiments comparable specimens were taken for electron microscopic examination as well. Fine structural alteration developed less uniformly and more slowly in A than in V. The most striking metabolic differences between A and V were: (1) A had a consistently higher tissue pH and lower lactate level (2) The sum of the adenine + hypoxanthine metabolites was essentially constant bu significantly different for each (A=5.04±0.12 (s.e.m.), V=7.71±0.15 (s.e.m.) μmol/g wet tissue weight) (3) Initial ATP levels were lower (40% less) in A (4) The maximum accumulation of AMP was higher in A, despite its smaller pool of adenine metabolites (5) Both adenosine and inosine showed slower rates of change in A. These results suggest that during early, severe ischaemic injury A and V show differing activities of 5′-nucleotidase.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-1803
    Keywords: reperfusion ; adenine ; nucleotides ; oxypurines ; electrolytes ; mechanicalwork
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Isolated rat hearts were used to measure tissue levels of the adenine nucleotides plus their degradation products and the ‘intracellular’ electrolytes after 15 or 25 min of global ischaemia alone and also after 5 or 60 min of reperfusion. Following 15 min of ischaemia, hearts showed near complete recovery of cardiac function (aortic flow rate =92±7% of control), but recovery was severely depressed following 25 min of ischaemia (aortic flow rate =18±15% of control). Similarly, after 5 min of reperfusion, hearts made ischaemic for 25 min had a reduced tissue content of ATP (10.5 vs 18.9 μmol·g·dry wt), and NAD (4.30 vs 4.75 μmol·g·dry wt) and a 3–4-fold increase in AMP, adenosine and oxypurines, as compared with hearts ischaemic for 15 min. However, the extent of loss of oxypurines during 5 min of reperfusion was essentially similar in both groups (21% vs 18% of total purine pool). After this initial period of reperfusion a significant (p〈0.01) difference in potassium content was seen between the two groups; hearts which recovered function gained, whilst failing hearts lost, potassium. Changes in the other electrolytes were essentially similar in the two groups of hearts. Extending reperfusion from 5 to 60 min did not change ATP levels in either group but in the functionally depressed group it was associated with a 5-fold increase in calcium and a 30% reduction in potassium, together with a further loss of oxypurines. Thus, loss of nucleotide precursors does not appear to be a critical event in the relatively sudden transition from reversible to irreversible functional injury in ischaemia. There may, however, be a reduction in the activity of the ATP synthesizing processes.
    Type of Medium: Electronic Resource
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