A selective suppression of human pain sensitivity by carbon dioxide: central mechanisms implicated

Abstract

The effect of breathing CO₂ on somatic sensitivity was studied in human subjects. Healthy humans breathed room air, 100% O₂, or CO₂ (5% or 8% in O₂). Thresholds to heat pain, mechanical pain, electrically evoked pain, and electrically evoked perception were measured using psychophysical techniques. Also, the effects on sensory and affective components of experimental ischaemic pain, alertness and on cardiovascular parameters were observed. In addition, the effect of C0₂ on heat pain threshold was determined in the ischaemic limb to exclude the possibility that the threshold elevation was due to an action on primary afferent fibres. Naloxone (0.8 mg), dexamethasone (0.1 mg) or placebo (0.9% NaCl) were applied intravenously in double blind tests to reverse the threshold elevations. In an electrophysiological experiment the effect of CO₂ on a spinal nociceptive flexion reflex evoked by an electric stimulus was measured. The CO₂ produced a dose-dependent elevation of the heat pain threshold. Similarly, the sensory and affective components of experimental ischaemic pain were attenuated by CO₂. The heat pain threshold was significantly elevated by CO₂ in the ischaemic limb, also. However, there was no effect on thresholds to mechanically or electrically induced pain or perception thresholds to electrically evoked sensations. One hundred percent O₂ did not elevate the heat pain threshold. In double blind tests the heat pain threshold elevation was not significant when the naloxone or dexamethasone was administered. The threshold to electrically evoked spinal flexion reflex was not elevated by CO₂. The CO₂ at the current dose produced sedation, an increase in blood pressure but no change in heart rate. The results would indicate that CO₂ (5%–8%) produces a dosedependent selective suppression of thermal and ischaemic pain due to central mechanisms. Stress-induced opioidergic mechanisms related to release of adenohypophyseal hormones may underly the suppression produced by CO₂ at the concentrations studied.