Attenuation of Pain in a Randomized Trial by Suppression of Peripheral Nociceptive Activity in the Immediate Postoperative Period
- 1 November 2002
- journal article
- clinical trial
- Published by Wolters Kluwer Health in Anesthesia & Analgesia
- Vol. 95 (5) , 1351-1357
- https://doi.org/10.1097/00000539-200211000-00047
Abstract
Peripheral neuronal barrage from tissue injury produces central nervous system changes that contribute to the maintenance of postoperative pain. The therapeutic approaches to blocking these central changes remain controversial, because previous studies have not differentiated presurgical interventions from those administered after tissue injury, yet before pain onset. In this study, we evaluated the relative contributions of blockade of nociceptive input during surgery or during the immediate postoperative period on pain suppression. Subjects were randomly allocated to one of four groups: preoperative 2% lidocaine, postoperative 0.5% bupivacaine, both, or placebo injections. General anesthesia was induced and third molars extracted. Pain was assessed over 4 h and at 24 and 48 h. The β-endorphin in blood samples increased twofold during surgery, which is indicative of activation of the peripheral nociceptive barrage in response to painful stimuli. Pain was decreased in the immediate postoperative period in the bupivacaine groups, whereas it increased in the lidocaine group over time. Pain intensity was less 48 h after surgery in the groups whose postoperative pain was blocked by the administration of bupivacaine, but no effect was demonstrated for the preoperative administration of lidocaine alone. These results in the oral surgery pain model suggest that minimizing the peripheral nociceptive barrage during the immediate postoperative period decreases pain at later time periods. In contrast, blocking the intraoperative nociceptive barrage does not appear to contribute significantly to the subsequent reduction in pain.Keywords
This publication has 33 references indexed in Scilit:
- The effects of a non-competitive NMDA receptor antagonist, MK-801, on behavioral hyperalgesia and dorsal horn neuronal activity in rats with unilateral inflammationPain, 1992
- The induction and maintenance of central sensitization is dependent onN-methyl-d-aspartic acid receptor activation; implications for the treatment of post-injury pain hypersensitivity statesPublished by Wolters Kluwer Health ,1991
- Central nervous system plasticity in the tonic pain response to subcutaneous formalin injectionBrain Research, 1990
- Postoperative Pain After Inguinal Herniorrhaphy with Different Types of AnesthesiaAnesthesia & Analgesia, 1990
- Expansion of receptive fields of spinal lamina I projection neurons in rats with unilateral adjuvant-induced inflammation: the contribution of dorsal horn mechanismsPain, 1989
- Subcutaneous formalin-induced activity of dorsal horn neurones in the rat: differential response to an intrathecal opiate administered pre or post formalinPain, 1987
- Dynamic receptive field plasticity in rat spinal cord dorsal horn following C-primary afferent inputNature, 1987
- Morphine-sensitive and morphine-insensitive actions of C-fibre input on the rat spinal cordNeuroscience Letters, 1986
- Slow excitatory transmission in rat dorsal horn: possible mediation by peptidesBrain Research, 1984
- Evidence for a central component of post-injury pain hypersensitivityNature, 1983