BACKGROUND: Although many studies show that pain increases breathing, they give little information on the mechanism by which pain interacts with ventilatory control. The authors quantified the effect of experimentally induced acute pain from activation of cutaneous nociceptors on the ventilatory control system. METHODS: In eight volunteers, the influence of pain on various stimuli was assessed: room air breathing, normoxia (end-tidal pressure of carbon dioxide (PET(CO2)) clamped, normoxic and hyperoxic hypercapnia, acute hypoxia, and sustained hypoxia (duration, 15-18 min; end-tidal pressure of oxygen, approximately 53 mmHg). Noxious stimulation was administered in the form of a 1-Hz electric current applied to the skin over the tibial bone. RESULTS: While volunteers breathed room air, pain increased ventilation (V(I)) from 10.9 +/- 1.7 to 12.9 +/- 2.5 l/min(-1) (P < 0.05) and reduced PET(CO2) from 38.3 +/- 2.3 to 36.0 +/- 2.3 mmHg (P < 0.05). The increase in V(I) due to pain did not differ among the different stimuli. This resulted in a parallel leftward-shift of the V(I)-carbon dioxide response curve in normoxia and hyperoxia, and in a parallel shift to higher V(I) levels in acute and sustained hypoxia. CONCLUSIONS: These data indicate that acute cutaneous pain of moderate intensity interacted with the ventilatory control system without modifying the central and peripheral chemoreflex loop and the central modulation of the hypoxia-related output of the peripheral chemoreflex loop. Pain causes a chemoreflex-independent tonic ventilatory drive.
BACKGROUND: Although many studies show that pain increases breathing, they give little information on the mechanism by which pain interacts with ventilatory control. The authors quantified the effect of experimentally induced acute pain from activation of cutaneous nociceptors on the ventilatory control system. METHODS: In eight volunteers, the influence of pain on various stimuli was assessed: room air breathing, normoxia (end-tidal pressure of carbon dioxide (PET(CO2)) clamped, normoxic and hyperoxic hypercapnia, acute hypoxia, and sustained hypoxia (duration, 15-18 min; end-tidal pressure of oxygen, approximately 53 mmHg). Noxious stimulation was administered in the form of a 1-Hz electric current applied to the skin over the tibial bone. RESULTS: While volunteers breathed room air, pain increased ventilation (V(I)) from 10.9 +/- 1.7 to 12.9 +/- 2.5 l/min(-1) (P < 0.05) and reduced PET(CO2) from 38.3 +/- 2.3 to 36.0 +/- 2.3 mmHg (P < 0.05). The increase in V(I) due to pain did not differ among the different stimuli. This resulted in a parallel leftward-shift of the V(I)-carbon dioxide response curve in normoxia and hyperoxia, and in a parallel shift to higher V(I) levels in acute and sustained hypoxia. CONCLUSIONS: These data indicate that acute cutaneous pain of moderate intensity interacted with the ventilatory control system without modifying the central and peripheral chemoreflex loop and the central modulation of the hypoxia-related output of the peripheral chemoreflex loop. Pain causes a chemoreflex-independent tonic ventilatory drive.