Effects of nitric oxide-donors and COX-2 inhibitors on nociceptive flexion reflex

G. Sandrini, A. Proietti Cecchini, E. Alfonsi, G. Nappi

Research output: Contribution to journalArticlepeer-review


Background. Central mechanism are involved not only in chronic pain states but even in transient acute nociceptive pain, as evidenced by studies on temporal summation of pain perception (wind-up). Several experimental studies suggest a pro-nociceptive role for nitric oxide. The recent discovery of a new inducible form of cyclooxygenase, the COX-2, already significantly expressed in CNS even in absence of inflammation, raises the question of additional benefit from a central analgesic effect by COX-2 inhibitors. Aims. To assess the effects of NO-donor and COX-2 inhibitor on spinal nociceptive flexion reflex (RIII). Materials and method. Nimesulide (100 mg p.o.), a preferential COX-2 inhibitor, and glycerin trinitrate (GTN) were given in a randomized, double-blind, placebo-controlled, cross-over study to 10 healthy drug-free volunteers (6 M, 4 F, mean age 29.8±7.6 yrs). The RIII reflex was elicited by electrical stimulation at the sural nerve and recorded from the biceps femoris. The study consisted of two sessions, placebo and active drug, separated by at least a 4-day interval. RIII area at 1.5 the threshold were obtained 15 min and then each 30 min after the tablet administration. Given the linear correlation between intensity of stimuli (i) and RIII area (A), we assumed the ratio A/i2 as index for monitoring the effects of GTN and nimesulide. Results. A reduction of A/i2 was observed starting from 15 min after nimesulide administration and revealed to be significant at 2 h when compared to placebo. After GTN, while the nimesulide group maintains the trend for an inhibitory effect, the placebo group shows a marked increase in A/i2, significant starting from 30 min up to 120 min (P

Original languageEnglish
JournalNeurological Sciences
Issue number4 SUPPL.
Publication statusPublished - 2000

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)


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