INFLUENCE OF ACUTE PAIN INDUCED BY ACTIVATION OF CUTANEOUS NOCICEPTORS ON VENTILATORY CONTROL

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 experim entally induced acute pain from activation of cutaneous nociceptors on the ventilatory control system.Methods: In eight volunteers, the infl uence of pain on various stimuli was assessed: room air breathing, nor moxia (end-tidal pressure of carbon dioxide (PETCO2) clamped, normoxic and hyperoxic hypercapnia, acute hypoxia, and sustained hypoxia (dura tion, 15-18 min; end-tidal pressure of oxygen, approximately 53 mmHg). Noxious stimulation was administered in the form of a 1-Hz electric c urrent applied to the skin over the tibial bone, Results: While volunt eers breathed room air, paint increased ventilation ((V) over dot(I)) from 10.9 +/- 1.7 to 12.9 +/- 2.5 1/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) over dot(I) due to pain did not differ among the different stimul i. This resulted in a parallel leftward-shift of the (V) over dot(I)-c arbon dioxide response curve in normoxia and hyperoxia, and in a paral lel shift to higher (V) over dot(I) levels in acute and sustained hypo xia. Conclusions: These data indicate that acute cutaneous pain of mod erate 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 chemorefle x loop, Pain causes a chemoreflex-independent tonic ventilatory drive.