Skip to main content
SpringerLink
Log in

Metabolic and haemodynamic responses to adrenaline in normal dogs

  • Original Contributions
  • Published:
Basic Research in Cardiology Aims and scope Submit manuscript

Summary

The metabolic and haemodynamic effects of adrenaline were investigated in 6 intact anaesthetized dogs, which were subjected to an infusion of adrenaline. The dose given was similar to the endogenous production rate of adrenaline in experimental myocardial infarction. Adrenaline infusion (0.8, 1.17 or 1.05μg · kg−1. min−1) over two hours led to a variable rise in blood level of this amine, regardless of the rate of infusion. Dogs with high blood adrenaline (over 3.5 ng·ml−1) exhibited haemodynamic deterioration, i.e a rise in peripheral vascular resistance together with a fall in cardiac output and external cardiac work. Dogs with low blood adrenaline showed little change in peripheral vascular resistance, a rise in cardiac output and external cardiac work. The myocardial consumption of each of the substrates lactate, pyruvate, glucose and FFA was measured, and its equivalent oxygen consumption expressed as a percentage of the total myocardial oxygen consumption. No relationship was found between myocardial utilisation of individual substrates and the type of haemodynamic response. Thus in intact dogs exposed to adrenaline excess, similar to that found in acute myocardial infarction, the different types of haemodynamic response cannot be attributed to the type of substrate utilization by the myocardium, but to different rates of clearance of adrenaline. Low clearance rates lead to high blood adrenaline levels and an unfavourable response of the cardiovascular system.

Zusammenfassung

An 6 narkotisierten Hunden wurden die metabolischen und hämodynamischen Auswirkungen einer Adrenalin-Infusion untersucht. Die Dosierung stimmte weitgehend mit der endogenen Produktionsrate von Adrenalin bei experimentellem Herzinfarkt überein. Eine Adrenalin-Infusion (0,8; 1,17 oder 1,05 μg/kg) über 2 Stunden führte zu einem variablen Anstieg des Blutspiegels von Adrenalin. Hunde mit einem hohen Blutspiegel (über 3,5 μg · kg−1 · min−1) zeigten hämodynamische Störungen, d. h. einen Anstieg des peripheren Widerstandes, verbunden mit einem Abfall des Herzminutenvolumens und der äußeren Herzarbeit. Hunde mit niedrigem Blutspiegel zeigten nur geringe Änderungen des peripheren Widerstandes sowie einen Anstieg des Herzminutenvolumens und der äußeren Herzarbeit. Der myokardiale Verbrauch der Substrate Laktat, Pyruvat, Glucose und freie Fettsäuren wurde gemessen und der äquivalente Sauerstoffverbrauch als Prozentsatz des gesamten myokardialen Sauerstoffverbrauchs ausgedrückt. Es wurde keine Beziehung zwischen myokardialer Utilisation der einzelnen Substrate und der Art der hämodynamischen Reaktion gefunden. Ähnlich wie beim akuten Myokardinfarkt können auch bei Hunden unter starkem Adrenalineinfluß die verschiedenen hämodynamischen Reaktionstypen nicht auf die Art der Substratutilisation im Myokard bezogen werden, sondern auf unterschiedliche Geschwindigkeiten der Adrenalin-Elimination. Niedrige Eliminationsgeschwindigkeit führt zu hohen Adrenalinblutspiegeln und ungünstigen Reaktionen des kardiovaskulären Systems.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

References

  1. Ceremuzynski, L.: Catecholamines in blood and urine, thyroid and adrenocortical function and insulin level in myocardial infarction with mild and severe course. Ann. Med. Sect. Pol. Acad. Sci.15, 111–160 (1970).

    Google Scholar 

  2. Richardson, J. A.: Plasma catecholamine concentrations in acute infarction. In: Coronary Heart Disease. Ed. by William Likoff and John H. Moyer (16, 273) Grune and Stratton (New York, 1963).

    Google Scholar 

  3. Ceremuzynski, L., K. Herbaczynska-Cedro, B. Broniszewska-Ardelt, J. Nauman, A. Nauman, B. Wozniewicz, J. Lawecki: Evidence for the detrimental effect of adrenaline infused to healthy dogs in doses imitating spontaneous secretion after coronary occlusion. Cardiovasc. Res.12, 179–183 (1978).

    PubMed  Google Scholar 

  4. Dole, V. P., H. Meinertz: Microdetermination of long-chain fatty acids in plasma and tissues. J. Biol. Chem.235, 2595–2599 (1960).

    PubMed  Google Scholar 

  5. Chlouverakis, C.: Parasympathomimetic agents and the metabolism of rat adipose tissue. Metabolism12, 936–940 (1963).

    PubMed  Google Scholar 

  6. Euler, V. S., I. Floding. A fluorimetric method for differential estimation of adrenaline and noradrenaline. Acta Physiol. Sc.33, suppl. 118, 45–52 (1955).

    Google Scholar 

  7. Maruchin, J., J. Olesinski: Spectrofluorometry in assay of urinary catecholamines. (In Polish) Diagn. Lab.14, 287–295 (1978).

    Google Scholar 

  8. Domenech, R. J., J. I. L. Hoffman, M. I. M. Noble, K. B. Saunders, J. T. Henson, S. Subijanto: Total and regional coronary blood flow measured by radioactive microspheres in conscious and anaesthetized dogs. Circulat. Res.25, 581–596 (1969).

    PubMed  Google Scholar 

  9. Van den Bos, G. C., A. J. Drake, M. I. M. Noble: The effect of carbon dioxide upon myocardial contractile performance, blood flow and oxygen consumption. J. Physiol.287, 149–161 (1979).

    PubMed  Google Scholar 

  10. Drake, A. J., J. R. Haines, M. I. M. Noble: Preferential uptake of lactate by the normal myocardium in dogs. Cardiovasc. Res.14, 65–72 (1980).

    PubMed  Google Scholar 

  11. Drake, A. J., D. E. Papadoyannis, R. G. Butcher, J. Stubbs, M. I. M. Noble: Inhibition of glycolysis in the denervated dog heart. Circulat. Res.47, 338–345 (1980).

    PubMed  Google Scholar 

  12. Kaijser, L., B. W. Lassers, M. L. Wahlqvist, L. A. Carlson: Myocardial lipid and carbohydrate metabolism in fasting men during prolonged exercise. J. Appl. Physiol.32, 847–858 (1972).

    PubMed  Google Scholar 

  13. Most, A. S., M. H. Lipsky, B. P. A. Szydlik, C. Bruno: Failure of FFA to influence myocardial oxygen consumption in the intact anaesthetized dog. Cardiology58, 220–228 (1973).

    PubMed  Google Scholar 

  14. Noble, M. I. M.: Left ventricular load, arterial impedance and their interrelationship. Cardiovasc. Res.13, 183–198 (1979).

    PubMed  Google Scholar 

  15. Wilcken, D. E. L., A. A. Charlier, J. I. E. Hoffman, A. Guz: Effects of alterations in aortic impedance on the performance of the ventricles. Circulat. Res.14, 283 (1964).

    PubMed  Google Scholar 

  16. Herbaczynska-Cedro, K.: The influence of adrenaline secretion on the enzymes in heart muscle after acute coronary occlusion in dogs. Cardiovasc. Res.4, 168–175 (1970).

    PubMed  Google Scholar 

  17. Fitzgerald, G. A., P. Barnes, C. A. Hamilton, C. T. Dollery: Circulating adrenaline and blood pressure: the metabolic effects and kinetics of infused adrenaline in man. Eur. J. Clin. Invest.10, 401–406 (1980).

    PubMed  Google Scholar 

  18. Mueller, H. S., S. M. Ayres: Metabolic responses of the heart in acute myocardial infarction in man. Amer. J. Cardiol.42, 363–371 (1978).

    PubMed  Google Scholar 

  19. Vetter, N. J., W. Adame, R. C. Strange, M. F. F. Oliver: Initial metabolic and hormonal response to acute myocardial infarction. Lancet1974/1, 284–289.

  20. Valori, C., M. Thomas, J. Shillingford: Free noradrenaline and adrenaline excretion in relation to clinical syndromes following myocardial infarction. Amer. J. Cardiol.20, 605–617 (1967).

    PubMed  Google Scholar 

  21. Januszewicz, W., M. Sznajderman, B. Wocial, J. Preibisz: Urinary excretion of free norepinephrine and free epinephrine in patients with acute myocardial infarction in relation to its clinical course. Amer. Heart J.76, 345–352 (1968).

    PubMed  Google Scholar 

  22. Hayashi, J. D., A. J. Moss, P. N. Yu.: Urinary catecholamine excretion in myocardial infarction. Circulation40, 473–481 (1969).

    PubMed  Google Scholar 

  23. Jequiez, E., C. Perret: Urinary excretion of catecholamines and their main metabolites after myocardial infarction: relationship to the clinical syndrome. Europ. J. Clin. Invest.1970/1, 77–83.

    Google Scholar 

  24. Ceremuzynski, L., M. Sandler: Augmented excretion of catecholamine metabolites in mild course of myocardial infarction (MI) and increased excretion of free catecholamines (CA) in complicated MI. Lack of inactivation of CA in severe MI? VIIIth World congress of Cardiology, Tokyo, 17th-23rd September. 1978.

Download references

Author information

Author notes

  1. A. J. Drake

    Present address: Midhurst Medical Research Institute, GU29 OBL, Midhurst, Sussex

Authors and Affiliations

  1. Medical Research Centre, Polish Academy of Sciences, Warsaw The Midhurst Medical Research Institute, Midhurst, West Sussex, England

    A. J. Drake, K. Herbaczynska-Cedro, W. Czarnecki & M. I. M. Noble

  2. Research Teaching Centre, Warsaw Medical School, Warsaw, Poland

    K. Herbaczynska-Cedro, L. Ceremuzynski & W. Czarnecki

Authors
  1. A. J. Drake
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. K. Herbaczynska-Cedro
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. L. Ceremuzynski
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. W. Czarnecki
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. M. I. M. Noble
    View author publications

    You can also search for this author in PubMed Google Scholar

Rights and permissions

Reprints and permissions

About this article

Cite this article

Drake, A.J., Herbaczynska-Cedro, K., Ceremuzynski, L. et al. Metabolic and haemodynamic responses to adrenaline in normal dogs. Basic Res Cardiol 77, 188–196 (1982). https://doi.org/10.1007/BF01908172

Download citation

  • Received:

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF01908172

Key words

Search

Navigation