Chemoreception pp 135-140 | Cite as

Neuromuscular Blocking Agents and Carotid Body Oxygen Sensing

  • Malin Jonsson
  • Sten G. E. Lindahl
  • Lars I. Eriksson
Conference paper
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 536)


Ventilatory depression is the leading cause behind anesthesia related postoperative morbidity and mortality worldwide (Lunnet al., 1983). Residual effects of muscle relaxants and general anesthetics are frequently associated with postoperative ventilatory failure and hypoxia. It is known that the ventilatory response to acute hypoxia is mainly mediated by afferent input from peripheral chemoreceptors of the carotid body and from the aortic arch. However, the mechanism behind oxygen sensing of the carotid bodies is not fully known. Recent studies show that hypoxia may block the leak-type potassium channel inducing a depolarisation of the cell membrane of the type I (glomus) cell. This seems to open voltage-gated calcium channels with an inward flux of calcium that result in a release of excitatory neurotransmitters. The activation of the type 1 cell chemotransmission causes an increased activity in the carotid sinus nerve (CSN) which finally gives rise to an increased ventilation.


Muscle Relaxant Carotid Body Peripheral Chemoreceptor Hypoxic Ventilatory Response Carotid Sinus Nerve 
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  1. Cardone, C., Szenohradszky, J., Yost, S., and Bickler, P. E. (1994).Anesthesiology80, 1155–61; discussion 29A.PubMedCrossRefGoogle Scholar
  2. Chiodini, F., Charpantier, E., Muller, D., Tassonyi, E., Fuchs-Buder, T., and Bertrand, D. (2001).Anesthesiology94, 643–51.PubMedCrossRefGoogle Scholar
  3. Cohen G, H. Z.-Y., Grailhe R, Gallego J, Gaultier C, Changeux J-P, Lagercrantz H. (2002).PNAS. Google Scholar
  4. Eriksson, L. I. (1996).Acta Anaesthesiol Scand40, 520–3.PubMedCrossRefGoogle Scholar
  5. Eriksson, L. I., Lennmarken, C, Wyon, N., and Johnson, A. (1992).Acta Anaesthesiol Scand36, 710–5.PubMedCrossRefGoogle Scholar
  6. Eriksson, L. I., Sato, M., and Severinghaus, J. W. (1993).Anesthesiology78,693–9.PubMedCrossRefGoogle Scholar
  7. Fitzgerald, R. S., Shirahata, M., and Wang, H. Y. (2000).Adv Exp Med Biol475,485–94.PubMedGoogle Scholar
  8. Igarashi, A., Amagasa, S., Horikawa, H., and Shirahata, M. (2002).Anesth Analg94, 117–22, table of contents.PubMedGoogle Scholar
  9. Ishizawa, Y., Fitzgerald, R. S., Shirahata, M., and Schofield, B. ( 1996).Adv Exp Med Biol410, 253–6.PubMedCrossRefGoogle Scholar
  10. Jonsson, M., Kim, C, Yamamoto, Y., Runold, M., Lindahl, S. G., and Eriksson, L. I. (2002).Acta Anaesthesiol Scand46, 488–94.PubMedCrossRefGoogle Scholar
  11. Lunn, J. N., Hunter, A. R., and Scott, D. B. (1983).Anaesthesia38, 1090–6.PubMedCrossRefGoogle Scholar
  12. Prabhakar, N. R. (2000).J Appl Physiol88, 2287–95.PubMedGoogle Scholar
  13. Shirahata, M., Ishizawa, Y., Rudisill, ML, Schofield, B., and Fitzgerald, R. S. (1998).Brain Res814,213–7.PubMedCrossRefGoogle Scholar
  14. Tassonyi, E., Charpantier, E., Muller, D., Dumont, L., and Bertrand, D. (2002).Brain Res Bull57, 133–50.PubMedCrossRefGoogle Scholar
  15. Wyon, N., Eriksson, L. I, Yamamoto, Y., and Lindahl, S. G. (1996).Anesth Analg82, 1252–6.Google Scholar
  16. Wyon, N., Joensen, H., Yamamoto, Y., Lindahl, S. G., and Eriksson, L. I. (1998).Anesthesiology89, 1471–9.PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 2003

Authors and Affiliations

  • Malin Jonsson
    • 1
  • Sten G. E. Lindahl
    • 1
  • Lars I. Eriksson
    • 1
  1. 1.Department of Anesthesiology and Intensive Care MedicineKarolinska Hospital and InstituteStockholmSweden

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