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Effect of myocardial oxygen consumption on infarct size in experimental coronary artery occlusion

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Summary

The influence of myocardial oxygen consumption (MVO2) at the moment of coronary occlusion on the size of the ensuing necrosis was investigated in 12 anaesthetised dogs. A two-infarction model was used with a sequential occlusion of two distant coronary branches in the same heart, however under different levels of MVO2. One group of occlusions was produced at a high MVO2 of 21.6±3.0 ml O2... min−1. 100 g−1. This group was compared with a second in which necrosis proceeded at a low MVO2 estimated to be 5.9±1.5 ml O2·min−1. 100 g−1 averaged over a 90-min occlusion period. Infarct size expressed as percentage of perfusion area was 43±28% in group 1 and 11±11% in group 2 (p<0.005). The mass of the perfusion area was equal in both groups (17±4 g, 19±6 g). The amount of myocardial necrosis, which after a 90-min occlusion depends on the acute collateral blood flow, was in every case greater under high MVO2. Thus a low MVO2 at the moment of occlusion can postpone myocardial necrosis.

Zusammenfassung

Der Einfluß des kardialen Sauerstoffverbrauchs (MVO2) auf die Infarktgröße wurde bei 12 narkotisierten Hunden untersucht. Zwei voneinander völlig getrennte Seitenäste der linken Koronararterie wurde nacheinander am selben Herzen verschlossen. Das erste Gefäßkollektiv wurde bei einem MVO2 von 21,6±3,0 ml ·min−1. 100 g−1 okkuldiert, das zweite bei einem MVO2 von 5,9±1,5ml·min−1 ·100g−1. Die Infarktgröße, ausgedrückt als Fraktion des Perfusionsgebietes, war 43±28% in Gruppe 1 und 11±11% in Gruppe 2 (p<0,005). Die Perfusionsgebiete, die okkludiert wurden, waren in beiden Gruppen gleich (17±4g, 19±6 g). Die Infarktgröße, die nach einer 90-min-Okklusion vom akuten Kollateralfluß abhängt, war in jedem Fall größer bei einem höheren MVO2. Somit kann ein, niedrigerer MVO2 zum Zeitpunkt des Verschlusses die Entwicklung der Nekrose zumindest hinauszögern.

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References

  1. Bloom, S., D. L. Davis: Calcium as mediator of isoproterenol induced myocardial necrosis. Amer J. Path69, 459 (1972).

    PubMed  Google Scholar 

  2. Bretschneider, H. J.: Die Determinanten des myokardialen Sauerstoffverbrauchs. In: Dengler, H. J. (ed.), Die therapeutische Anwendung β-sympathikolytischer Stoffe, pp. 45, Schattauer Verlag (Stattgart 1971).

    Google Scholar 

  3. Genth, K., M. Hofmann, M. Hofmann, W. Schaper: The effect of β-adrenergic blockade on infarct size following experimental coronary occlusion. Basic Res. Cardiol.76, 144 (1981).

    PubMed  Google Scholar 

  4. Hofmann, M., M. Hofmann, K. Genth, W. Schaper: The influence of reperfusion on infarct size after experimental coronary artery occlusion. Basic Res. Cardiol.75, 572 (1980).

    PubMed  Google Scholar 

  5. Holland, R. P., H. Brooks: TQ-ST mapping: critical review and analysis of current concepts. Amer. J. Cardiol.40, 110 (1977).

    PubMed  Google Scholar 

  6. Jennings, R. B., K. A. Reimer: Effect of beta-adrenergic blockade on acute myocardial ischemic injury. In: Modulation of Sympathetic Tone in the Treatment of Cardiovascular Diseases, pp. 103, (Ed. F. Gross) (Bern 1979).

  7. Kirk, E. S., H. O. Hirzel, E. H. Sonnenblick: The relative role of supply and demand in the effect of isoproterenol on infarct size. Circulation55 and56 (Suppl 3): III 149, Ref. 571 (1977).

    Google Scholar 

  8. Klein, H. H., J. Schaper, W. Schaper: Study on the mechanism of tetrazolium salts in identifying experimental myocardial infarction. Z. Kardiol.70, 316, P 233 (1981).

    Google Scholar 

  9. Levken, J., C. Semb: Effect of dopamine and of calcium on lipolysis and on myocardial ischemic injury following acute coronary artery occlusion in the dog. Circulat. Res.34, 349 (1974).

    PubMed  Google Scholar 

  10. Maroko, P. R., J. K. Kjekshus, B. E. Sobel, T. Watanabe, J. W. Covell, J. Jr. Ross, E. Braunwald: Factors influencing infarct size following experimental coronary artery occlusion. Circulation43, 67 (1971).

    PubMed  Google Scholar 

  11. Marshall, R. J., J. R. Parratt: The effect of noradrenaline on blood flow and oxygen consumption in normal and ischemic areas of myocardium. Amer. Heart J.86, 653 (1973).

    PubMed  Google Scholar 

  12. Mjos, O. D., J. K. Kjekshus, J. Levken: Importance of free fatty acids as a determinant of myocardial oxygen consumption and myocardial ischemic injury during norepinephrine infusions in dogs. J. Clin. Invest.53, 1290 (1974).

    PubMed  Google Scholar 

  13. Müller, K. D., H. Klein, W. Schaper: Changes in myocardial oxygen consumption 45 minutes after experimental coronary occlusion do not alter infarct size. Cardiovasc. Res.14, 710 (1980).

    PubMed  Google Scholar 

  14. Norris, R. M., H. J. Smith, B. N. Singh, H. Nisbet, M. B. John, P. J. Hurley: The effects of isoprenaline on epicardial S-T segment elevation, lactate production and myocardial blood flow following coronary artery ligation. Cardiovasc. Res.9, 770 (1975).

    PubMed  Google Scholar 

  15. Reid, P., B. Pitt, D. Kelly: Effects of dopamine on increasing infarct area in acute myocardial infarction. Circulation46 (Suppl. II), 210 (1972).

    Google Scholar 

  16. Rudolph, A. M., M. A. Heyman: The circulation of the fetus in utero: Methods for studying distribution of blood flow, cardiac output, and organ blood flow. Circulation Res.21, 163 (1967).

    PubMed  Google Scholar 

  17. Schaper, W., P. Lewi, W. Flameng, L. Gijpen: Myocardial steal produced by coronary vasodilatation in chronic coronary artery occlusion. Basic Res. Cardiol.68, 3 (1973).

    PubMed  Google Scholar 

  18. Schaper, W., H. Frenzel, W. Hort: Experimental coronary artery occlusion I. Measurement of infarct size. Basic Res. Cardiol.74, 46 (1979).

    PubMed  Google Scholar 

  19. Schaper, W., M. Hofmann, K. D. Müller, K. Genth, M. Carl: Experimental occlusion of two small coronary arteries in the same heart. A new validation method for infarct size manipulation. Basic Res. Cardiol.75, 224 (1979).

    Google Scholar 

  20. Schaper, W.: The relationship between collateral blood flow, myocardial oxygen consumption and infarct size. In: Schaper, W. (ed.), The Pathophysiology of Myocardial Perfusion, pp. 352. Elsevler/North-Holland Biomedical Press, (New York, Amsterdam, Oxford 1979).

    Google Scholar 

  21. Shell, W. E., B. E. Sobel: Deleterious effects of increased heart rate on infarct size in the conscious dog. Amer. J. Cardiol.31, 474 (1973).

    PubMed  Google Scholar 

  22. Tuttle, R. R., G. D. Pollock, G. Todd, B. M. McDonald, R. Tust, W. Dusenberry: The effect of dobutamine on cardiac oxygen balance, regional blood flow, and infarction severity after coronary artery narrowing in dogs. Circulat. Res.41, 357 (1977).

    PubMed  Google Scholar 

  23. Willerson, J. T., I. Hutton, J. T. Watson, M. R. Platt, G. H. Templeton: Influence of dobutamine on regional myocardial blood flow and ventricular performance during acute and chronic myocardial ischemia in dogs. Circulation53, 828 (1976).

    PubMed  Google Scholar 

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Müller, K.D., Sass, S., Gottwik, M.G. et al. Effect of myocardial oxygen consumption on infarct size in experimental coronary artery occlusion. Basic Res Cardiol 77, 170–181 (1982). https://doi.org/10.1007/BF01908170

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