Nociceptive flexion reflex responses were significantly attenuated during systole compared to diastole, supporting the arterial baroreflex mechanism of hypertensive hypoalgesia.
Does arterial baroreceptor stimulation during systole reduce nociceptive flexion reflex in normotensive adults?
Natural changes in blood pressure during the cardiac cycle dampen nociception, supporting the arterial baroreflex mechanism of hypertensive hypoalgesia.
Carotid baroreceptor stimulation has been shown to dampen pain. This study tested, in 40 normotensive adults, the hypothesis that pain is lower during systole when arterial baroreceptor stimulation is maximal than diastole when stimulation is minimal. The sural nerve was stimulated electrocutaneously to obtain a nociceptive flexion reflex (NFR) threshold, and then stimulation was delivered for 28 trials at 100% NFR threshold at seven intervals after the R-wave. Nociceptive responding was indexed by electromyographic (EMG) activity elicited in the biceps femoris. Significant variations in EMG activity occurred across the cardiac cycle, with less activity midcycle, indicating that the NFR response was attenuated during systole compared to diastole. Stimulation of baroreceptors by natural changes in blood pressure during the cardiac cycle dampened nociception, and accordingly, the data support the arterial baroreflex mechanism of hypertensive hypoalgesia.
Edwards et al. (Sun,) reported a other. Systole (maximal arterial baroreceptor stimulation) vs. Diastole (minimal stimulation) was evaluated on Nociceptive flexion reflex (NFR) indexed by electromyographic (EMG) activity. Nociceptive flexion reflex responses were significantly attenuated during systole compared to diastole, supporting the arterial baroreflex mechanism of hypertensive hypoalgesia.