2006, Number 1
<< Back Next >>
Rev Mex Anest 2006; 29 (1)
NSAIDs: their mechanism of action upon the central nervous system
Rivera-Ordóñez A
Language: Spanish
References: 19
Page: 36-40
PDF size: 117.11 Kb.
ABSTRACT
Non-steroidal anti-inflammatory drugs (NSAIDs) form a wide group of drugs, with shared therapeutic actions and side effects. NSAIDs have various central and peripheral effects, most of which are mediated through the inhibition of prostaglandin (PG) synthesis. Their analgesic effect is based on the blockade of the peripheral and central production of prostaglandins; at the central level, the sensitization of spinal and supraspinal neurons is prevented, allowing for the modulation (inhibition) of pain. Previous research on the central nervous system (CNS) and the activity of inflammatory cells, enzyme liberation, and free radicals derived from oxygen and other mechanisms, reveal that the effects of NSAIDs may be independent from prostaglandin synthesis. Considering all the aforementioned, plus the fact that cyclooxygenase inhibitors can be useful to considerably reduce pain and inflammation, these drugs are essential for the control of acute and chronic pain, and for preventing or reducing nociceptive impulses, by giving them both before and after soft tissue injury.
REFERENCES
Valdivieso SA. Dolor agudo, analgesia y sedación en el niño: farmacocinética y farmacodinamia de los analgésicos no opioides. Anales Españoles Pediátricos 1998;48:183-194.
McCormack K. Non-steroidal anti-inflammatory drug and spinal nociceptive processing. Pain 1994;59:9-43.
Goodman, Gilman. Las bases farmacológicas de la terapéutica. Novena edición. McGraw-Hill Interamericana 1996;1:661-669.
Goetzl EJ, An S, Smith WL. Specificity of expression and effects of eicosanoid mediators in normal physiology and human diseases. FASEB J 1995;9:1051-58.
Cashman J, Mc Anulty G. Nonsteroidal anti-inflammatory drugs in perisurgical pain management. Drugs 1995;49:51-70.
Kassian RA. Los analgésicos antiinflamatorios no esteroideos. Dolor, clínica y tratamiento 2002;2:5-10.
Venegas H, Schaible HG. 2001. Prostaglandins and cycloxygenases in the spinal cord. Progr Neurobiol, (in press).
Bhatt-Metha. Current guidelines for the treatment of acute pain in children. Drugs 1996;51:760-776.
Launes LJ. Nonsteroidal anti-inflammatory Drugs: use and the risk for Alzheimer’s disease. Drugs 2003;63:731-739.
Fiebicb BL, Hull M, et al. Prostaglandin E2 induces interleukin-6 synthesis in human astrocytoma cells. J Neuro Chem 1997;68:704-709.
BjorKman R. Central antinociceptive effects of non-steroidal anti-inflammatory drugs and paracetamol. Experimental studies in rat. Act Anaesth Scand 1995;103:1-44.
Brune K, et al. Aspirine-like drugs, may block pain independently of prostaglandin synthesis inhibition. Experentia 47:257-261.
Morgan L. Discussion in neuroscience: proto-oncogene expression in the nervous system. Elsevier, Amsterdam. 1991;VII(4).
Salvemini D, Manning PI, Zweifel BS, et al. Dual inhibition of nitric oxide and prostaglandin production contributes to the anti-inflammatory properties of nitric oxide synthase inhibitors. J Clin Invest 1995;96:301-308.
Acunna MM. Mecanismo de acción de los analgésicos antiinflamatorios no opioides. (ANOP). Capítulo Uruguayo de la IAPS. 2002:1-7.
Kaufmann WE, Andreasson KI, Isakson PC, et al. Ciclooxygenases and the central nervous system. Prostaglandins 1997;54:601-624.
Bannwarth B, Demotesmainard F, Schaverbeke T. Where are peripheral analgesics acting? Annals Rheumatics Disease 1993;52:1-4.
Ferreira SH. Prostaglandins: Peripheral and Central Analgesia. Advances in pain research and therapy. 1983;5:627-634.
Ferreiras SH. The role of interlevkins and nitric oxide in the mediation of inflammatory pain and its control by peripheral analgesics. Drugs 1993;46:1-9.