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1 Laboratoire de Physiopathologie Respiratoire, Service de Pneumologie, Groupe Hospitalier Pitie Salpetriere, Assistance Publique Hopitaux de Paris, Paris, France; UPRES EA 2397, Universite Paris 6, Paris, France
2 UPRES EA 2397, Universite Paris 6, Paris, France; Service Central d Explorations Fonctionnelles Respiratoires, Groupe Hospitalier Pitie Salpetriere, Assistance Publique Hopitaux de Paris, Paris, France
3 Federation de Neurophysiologie Clinique and INSERM U731, Groupe Hospitalier Pitie Salpetriere, Assistance Publique Hopitaux de Paris, Paris, France
4 Laboratoire de Physiopathologie Respiratoire, Service de Pneumologie, Groupe Hospitalier Pitie Salpetriere, Assistance Publique Hopitaux de Paris, Paris, France
* To whom correspondence should be addressed. E-mail: thomas.similowski{at}psl.ap-hop-paris.fr.
Dyspnea, a leading respiratory symptom, shares many clinical, physiological and psychological features with pain. Both activate similar brain areas. The neural mechanisms of dyspnea are less well described than those of pain. The present research tested the hypothesis of common pathways between the two sensations. Six healthy men (age 30-40) were studied. The spinal nociceptive flexion reflex (RIII) was first established in response to electrical sural stimulation. Dyspnea was then induced through inspiratory threshold loading, forcing the subjects to develop 70% of their maximal inspiratory pressure to inhale. This led to progressive inhibition of the RIII reflex that reached 50 +/- 12% during the fifth minute of loading (P < 0.001), was correlated to the intensity of the self-evaluated respiratory discomfort, and had recovered 5 minutes after removal of the load. The myotatic H-reflex was not inhibited by inspiratory loading, arguing against post-synaptic alpha motoneurons inhibition. Dyspnea, like pain, thus induced counterirritation, possibly indicating at C-fiber stimulation and activation of diffuse noxious inhibitory descending controls known to project onto spinal dorsal horn wide dynamic range neurons. This confirms the noxious nature of certain types of breathlessness, hence opening new physiological and perhaps therapeutic perspectives.
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