• Amadeu Quelhas Martins, Christopher Ring, David McIntyre, Louisa Edwards, and Una Martin.
• International Centre for Health & Exercise Research, University of Birmingham, Birmingham, UK. amm626@bham.ac.uk
• Pain. 2009 Dec 15;147(1-3):84-90.

AbstractPrevious research has demonstrated that the nociceptive flexion reflex (NFR) and pain-related evoked potentials are reduced in amplitude when elicited during the middle of the cardiac cycle. Despite these findings, suggesting a baroreceptor mechanism of antinociception during systole, pain intensity ratings reported in these studies were not modulated across the cardiac cycle. This discrepancy between the neurophysiological correlates of pain and its subjective experience was the focus of the current study that used a mixed block design to assess the effects of natural arterial baroreceptor activity on both the NFR and pain intensity and unpleasantness reports. Specifically, electrocutaneous stimuli were randomly delivered to the sural nerve at one of five intensities (50% pain threshold, 75% pain threshold, pain threshold, midway between pain threshold and pain tolerance, pain tolerance) at five intervals (0, 150, 300, 450, and 600ms) after the R-wave of the electrocardiogram. Under painful stimulation, intensity and unpleasantness varied in a quadratic manner across the cardiac cycle; pain was highest at R+300ms and lowest at R+0 and R+600ms. Under non-painful stimulation, ratings declined linearly as the cycle progressed. Finally, nociceptive responses did not differ among the R-wave to stimulation intervals for both painful and non-painful intensities. The observed phasic modulation of pain may be explained by a central nervous system alarm/defence reaction triggered by the unpredictability of the potentially damaging stimulation. The absence of systolic attenuation of nociceptive responding is compatible with previous evidence that baroreceptor modulation of the NFR is abolished under conditions of heightened arousal.

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