Intravenous adenosine activates diffuse nociceptive inhibitory controls in humans

Author:

Morélot-Panzini Capucine12,Corvol Jean-Christophe34,Demoule Alexandre12,Raux Mathieu25,Fiamma Marie-Noëlle12,Willer Jean-Claude56,Similowski Thomas12

Affiliation:

1. Assistance Publique - Hôpitaux de Paris, Groupe Hospitalier Pitié Salpêtrière Charles Foix, Service de Pneumologie et Réanimation Médicale, Paris, France;

2. Université Paris 6, ER10UPMC, Paris, France;

3. Assistance Publique - Hôpitaux de Paris, Groupe Hospitalier Pitié Salpêtrière Charles Foix, Département de Neurologie, Département de Pharmacologie, INSERM CIC-9503, Paris, France;

4. INSERM UMRS975 UPMC, CNRS UMR 7225, CR ICM, Pitié-Salpêtrière, Paris, France;

5. Assistance Publique - Hôpitaux de Paris, Groupe Hospitalier Pitié Salpêtrière Charles Foix, Département d'Anesthésie et Réanimation, Paris, France; and

6. Assistance Publique - Hôpitaux de Paris, Groupe Hospitalier Pitié Salpêtrière Charles Foix, Département de Neurophysiologie Clinique, Paris, France

Abstract

Experimentally induced pain can be attenuated by concomitant heterotopic nociceptive stimuli (counterirritation). Animal data indicate that this stems from supraspinal “diffuse noxious inhibitory controls” (DNICs) triggered by C and Aδ fibers. In humans, only noxious stimuli induce counterirritation. This points at C fibers, but the effects of pharmacologically stimulating C fibers have not been studied. Intravenous adenosine activates pulmonary C fibers and induces dyspnea. This study tests the hypothesis that putative activation of pulmonary C fibers by adenosine would trigger DNICs in humans and induce counterirritation. Twelve healthy volunteers were included (with valid results available in 9) and studied according to a double-blind, randomized, cross-over design (intravenous adenosine, 140 μg·kg−1·min−1, during 5 min vs. placebo). We measured ventilatory variables and end-tidal CO2 tension, dyspnea intensity by visual analog scale, and the intensity of putative chest pain. The primary outcome was the amplitude of the RIII component of the nociceptive flexor reflex recorded by biceps femoris electromyogram in response to painful electrical sural nerve stimulation (RIII), taken as a substitute for pain perception. Placebo did not induce any significant effect. Adenosine induced dyspnea, hyperpnea, tachycardia, and significant RIII inhibition (24 ± 8% at the 4th min, P < 0.0001). The temporal dynamics of adenosine-induced dyspnea and RIII inhibition differed (immediate onset followed by a slow decrease for dyspnea, slower onset for RIII inhibition). Intravenous adenosine in normal humans induces counterirritation, fueling the notion that C-fiber stimulation trigger DNICs in humans. The temporal dissociation between adenosine-induced dyspnea and RIII inhibition suggests that C fibers other than pulmonary ones might be involved.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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