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Nylidrin HCL: A beta-sympathetic stimulant in the management of haemorrhagic shock

  • Guy M. Boiteau
  • Jean-Paul Dechêne
Article
  • 118 Downloads

Summary

In the assessment of classical haemorrhagic shock in twenty-two dogs, thirteen of them treated with Nylidrin HC1, ten survived extended episodes of arterial hypotension down to a mean arterial pressure of 40 mm.Hg. Of nine control animals (untreated), five survived the re-infusion period. In the course of our study, Nylidrin HC1 displayed two important pharmacodynamic effects:
  1. 1.

    It stimulated peripheral tissue arterial inflow, thus assisting metabolic exchange and reducing the peripheral anoxia of circulatory failure which aggravates metabolic acidosis.

     
  2. 2.

    It significantly increased cardiac output. Nylidrin HC1 improves myocardial contractility and reduces peripheral arterial resistance. Slight increases in cardiac rate were also noted, along with a moderate decrease in arterial blood pressure. However, neither change proved to be statistically significant. Both groups were compared during and after shock to evaluate contributions to therapy afforded by a Beta stimulatory sympathomimetic. agent.

     

Keywords

Cardiac Output Blood Volume Arterial Blood Pressure Metabolic Acidosis Total Peripheral Resistance 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Résumé

Les résultats de cette étude sur le choc hémorragique chez vingt-deux chiens ont démontré que dix d’entre eux, traités par l’hydrochlorure de Nylidrin (77%), ont survécu des épisodes d’hypotension artérielle sévère de 40 mm.Hg (moyenne). Du groupe témoin composé de neuf chiens, cinq ont survécu sans traitement. Dans notre 6tude, ce médicament a eu deux actions pharmaco-dynamiques importantes:
  1. 1.

    D’augmenter le débit sanguin capillaire périphérique, tout en augmentant les échanges métaboliques et diminuant l’anoxie stagnante prolongéed qui aggrave l’acidose métabolique.

     
  2. 2.

    II augmente le débit cardiaque de façon significative. L’hydrochlorure de Nylidrin augmente la contractilité du myocarde et diminue la resistance artérielle périphérique. L’on note aussi qu’il y a une légère augmentation du pouls cardiaque et une légère diminution de la tension artérielle moyenne; toutefois, ces changements ne se sont avérés que peu significatifs. Les deux groupes ont été comparés avant, pendant et après le choc hémorragique pour éValuer l’action thérapeutique d’un agent bêta-sympathomimétique.

     

References

  1. 1.
    Vick, J. A.);Ciuchta, H. P.);Merickel, J. H.);et al.) Vasodilator Therapy in Acute Hemorrhagic Shock. Circ. Res.16: 58 (1965).PubMedGoogle Scholar
  2. 2.
    Danoff, D. S.) &Gheene, N. M.) Vasodilation and the Metabolic Response to Hemorrhage. Surgery55: 820 (1964).PubMedGoogle Scholar
  3. 3.
    Talaat, S. M.);Massion, W. H.); &Schilling, J. A.) Effects of Adenosine Triphosphate Administration in Irreversible Hemorrhagic Shock. Surgery55: 813 (1964).PubMedGoogle Scholar
  4. 4.
    Ahlquist, R. P.) A Study of the Adrenotropic Receptors. Am. J. Physiol.153: 586 (1948).PubMedGoogle Scholar
  5. 5.
    Rosenblum, W. I.) &Zweifach, B. W.) Cerebral Microcirculation in the Mouse Brain. Arch, of Neurol.9: 414 (1963).Google Scholar
  6. 6.
    DechEne, J. P.);Hebert, C.); &McClish, A.) Halothane-Ether in Cardiac Surgery. Can. Anaesth. Soc. J.9: 61 (1962).PubMedCrossRefGoogle Scholar
  7. 7.
    DechEne, J. P.) &Hebert, C.) Fluothane-Ether in Anaesthesia for Pulmonary Surgery. Can. Anaesth. Soc. J.7: 100 (1960).PubMedCrossRefGoogle Scholar
  8. 8.
    Hamilton, W. F.) Studies on the Circulation: IV. Further Analysis of the Injection Method, and of Changes in Hemodynamics Under Physiologic and Pharmacologic Conditions. Am. J. Physiol.99: 534 (1932).Google Scholar
  9. 9.
    Siggaard-Andersen, O.) Blood Acid-Base Alignment Nomogram. Scand. J. Clin. Lab. Invest.15: 211 (1963).CrossRefGoogle Scholar
  10. 10.
    Courtice, F. C.) The Blood Volume of Normal Animals. J. Physiol.102: 290 (1943).PubMedGoogle Scholar
  11. 11.
    MacLean, L. D.);Duff, J. H.);Scott, H. M.); &Peretz, D. I.) Treatment of Shock in Man Based on Hemodynamic Diagnosis. Surg. Gynec. & Obst.120: 1 (1965).Google Scholar
  12. 12.
    Downing, S. E.);TalneH, N. S.); &Gardner, T. H.) Cardiovascular Responses to Metabolic Acidosis. Am. J. Physiol.208: 237 (1965).PubMedGoogle Scholar
  13. 13.
    Peretz, D. I.);McGregor, M.); &Dossetor, J. B.) Lacticacidosis: A Clinically Significant Aspect of Shock. Canad. M.A.J.90: 673 (1964).Google Scholar
  14. 14.
    Korein, Tulrus. Effects of a Vasoactive Drug (Nylidrin HCl) on the Response of Electroencephalogram to Hyperventilation. Arch. Neurol. In press.Google Scholar
  15. 15.
    Whittier, J. R. &Dhoymiotis, A. The Effect of Cyclandelate, Isoxsuprine and Nylidrin on Hyperventilation Build up in the Electroencephalogram of Volunteer Subjects. Angiology16, no. 10 (1965).Google Scholar
  16. 16.
    Teller, F. (Arlington-Funk Laboratories). Personal Communication.Google Scholar

Copyright information

© Canadian Anesthesiologists 1966

Authors and Affiliations

  • Guy M. Boiteau
    • 1
  • Jean-Paul Dechêne
    • 2
  1. 1.Cardiac LaboratoryInstitute of Cardiology, Hôpital LavalQuebec
  2. 2.Department of AnesthesiaHôpital LavalQuebec

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