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Comparative biochemistry and fine structure of atrial and ventricular myocardium during autolysis in vitro

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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. (1)

    A had a consistently higher tissue pH and lower lactate level

  2. (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. (3)

    Initial ATP levels were lower (40% less) in A

  4. (4)

    The maximum accumulation of AMP was higher in A, despite its smaller pool of adenine metabolites

  5. (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.

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Author notes

  1. L. C. Armiger

    Present address: Department of Pathology, University of Auckland school of Medicine, Private Bag, Auckland, New Zealand

Authors and Affiliations

  1. Department of Pathology, University of Auckland school of Medicine, Private Bag, Auckland, New Zealand

    R. N. Seelye, M. A. Morrison & D. G. Holliss

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  1. L. C. Armiger
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  2. R. N. Seelye
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  3. M. A. Morrison
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  4. D. G. Holliss
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Armiger, L.C., Seelye, R.N., Morrison, M.A. et al. Comparative biochemistry and fine structure of atrial and ventricular myocardium during autolysis in vitro. Basic Res Cardiol 79, 218–229 (1984). https://doi.org/10.1007/BF01908308

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  • DOI: https://doi.org/10.1007/BF01908308

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