Abstract
The potent respiratory depressant effects of exogenous opiates are well known. Morphine and other opiates reduce ventilation, the ventilatory responses to hypercapnia and hypoxia, as well as the respiratory compensation for an acute increase in airway resistance.1-3 The discovery of endogenous opioid peptides such as beta-endorphin and enkephalin led to investigations into the possible role of these peptides in ventilatory control in humans. In one such study Santiago and co-workers found that the opioid antagonist naloxone restored the respiratory compensation for a flow-resistive load in those patients with chronic obstructive pulmonary disease in whom it was found to be absent.4 They postulated that in these patients endogenous opioids were elaborated in response to the stress of chronically increased airway resistance resulting in attenuation of compensation for the flow-resistive load. In a subsequent study in an unanesthetized goat model we tested the hypothesis that shorter periods of stress produced by increased airway resistance would activate the endogenous opioid system and reduce the subsequent ventilatory response.5 We found in animals exposed to two and one-half hours of inspiratory flow-resistive loading that the reduction in tidal volume was partially reversed by naloxone given at the conclusion of the loading period and that levels of immunoreactive beta-endorphin measured in the cisternal cerebrospinal fluid were increased. Our subsequent studies have been directed at defining the effect of activation of the endogenous opioid system on central respiratory output to the respiratory muscles and the peripheral signal responsible for the activation of this system. The results of these studies are discussed in detail below.
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsPreview
Unable to display preview. Download preview PDF.
References
J.V. Weil, R.E. McCullough, J.S. Kline, and I.E. Sodal, Diminished ventilatory response to hypoxia and hypercapnia after morphine in normal man, N. Engl. J. Med. 292:1103 (1975).
T.V. Santiago, K. Goldblatt, K. Winters, A. Pugliese, and N.H. Edelman, Respiratory consequences of methadone: the response to added resistance to breathing, Am. Rev. Respir. Dis. 122:623 (1980).
M.H. Kryger, O. Yacoub, J. Dosman, P.T. Macklem, and N.R. Anthonisen, Effect of meperidine on occlusion pressure responses to hypercapnia and hypoxia with and without external inspiratory resistance, Am. Rev. Respir. Dis. 114:333 (1976).
T.V. Santiago, C. Remolina, V. Scoles, and N.H. Edelman, Endorphins and control of breathing, N. Engl. J. Med. 304:1190(1981).
A.T. Scardella, R.A. Parisi, D.K. Phair, T.V. Santiago, and N.H. Edelman, The role of endogenous opioids in the ventilatory response to acute flow-resistive loads, Am. Rev. Respir. Dis. 133:26 (1986).
A.T. Scardella, T.V. Santiago, and N.H. Edelman, Naloxone alters the early response to an inspiratory flow-resistive load, J. Appl. Physiol. 67:1141 (1989).
A.T. Scardella, J.J. Petrozzino, M. Mandel, N.H. Edelman, and T.V. Santiago, Endogenous opioid effects on abdominal muscle activity during inspiratory loading, J. Appl. Physiol. 69:1104(1990).
J.J. Petrozzino, A.T. Scardella, T.V. Santiago, and N.H. Edelman, Dichloroacetate blocks endogenous opioid efffects during inspiratory flow-resistive loading, J. Appl. Physiol. 72:590 (1992).
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1992 Springer Science+Business Media New York
About this chapter
Cite this chapter
Scardella, A.T., Santiago, T.V., Edelman, N.H. (1992). The Role of Endogenous Opioids in the Ventilatory Response to Sustained Respiratory Loads. In: Honda, Y., Miyamoto, Y., Konno, K., Widdicombe, J.G. (eds) Control of Breathing and Its Modeling Perspective. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9847-0_35
Download citation
DOI: https://doi.org/10.1007/978-1-4757-9847-0_35
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4757-9849-4
Online ISBN: 978-1-4757-9847-0
eBook Packages: Springer Book Archive