[Effect of local anesthetics on the postoperative inflammatory response].
Current knowledge suggests that peripheral inflammation following surgery activates and sensitizes both peripheral and central nervous system. These phenomena involved in the maintenance of the inflammatory response lead to hypersensibility, hyperalgesia and allodynia. Hyperalgesia participates in the general experience of postoperative pain and ALo in the development of chronic pain. A correlation between the ability of treatments to reduce areas of hypersensitivity surrounding the wound after surgery and their ability to reduce the incidence of chronic pain has been shown. For a long time, local anaesthetics have been used for their capacity to block nociceptive input. They can ALo modulate the inflammatory response following a surgical trauma. By inhibiting the nervous conductivity at the site of the trauma, local anesthetics attenuate the sensitization of the nervous system and therefore the inflammatory phenomena. They ALo exert intrinsic anti-inflammatory properties by modulating the local and systemic liberation of inflammatory mediators. The mechanisms involved are not clearly elucidated. Local, systemic, and spinal inflammatory mechanisms may be influenced by local anesthetics through multiple different mechanisms. The therapeutic implications of effects of local anesthetics on local, systemic, and spinal inflammatory responses merit further study.
Beloeil
H
H
Département d'anesthésie-réanimation, hôpital de Bicêtre, AP-HP, université Paris-Sud, 78 avenue du Général-Leclerc, Le Kremlin-Bicêtre, France. helene.beloeil@bct.aphp.fr
Mazoit
J-X
JX
D000344:Afferent Pathways / Q000187:drug effects / Q000503:physiopathology; D015360:Analgesia, Epidural; D000779:Anesthetics, Local / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D001370:Axonal Transport / Q000187:drug effects; D002908:Chronic Disease / Q000517:prevention & control; D015232:Dinoprostone / Q000378:metabolism; D055724:Electrophysiological Phenomena / Q000187:drug effects; D006801:Humans; D006930:Hyperalgesia / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D007249:Inflammation / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000378:metabolism; D007262:Infusions, Intravenous; D020935:MAP Kinase Signaling System / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects; D009407:Nerve Block; D009420:Nervous System / Q000187:drug effects* / Q000503:physiopathology; D010149:Postoperative Pain / Q000188:drug therapy / Q000503:physiopathology / Q000517:prevention & control; D011183:Postoperative Complications / Q000503:physiopathology*; D051381:Rats; D043562:Receptors, G-Protein-Coupled / Q000187:drug effects; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects
D000779:Anesthetics, Local; D000894:Anti-Inflammatory Agents, Non-Steroidal; D018836:Inflammation Mediators; D043562:Receptors, G-Protein-Coupled; D016194:Receptors, N-Methyl-D-Aspartate; D015232:Dinoprostone