Acetaminophen prevents hyperalgesia in central pain cascade
| Autor: | Xiao-Ying Hua, B. K Crawley, Tony L. Yaksh, Osamu Saito, Bethany Fitzsimmons, Shelle Malkmus |
|---|---|
| Rok vydání: | 2008 |
| Předmět: |
Male
Analgesic Administration Oral Pain Substance P Pharmacology Dinoprostone Article Rats Sprague-Dawley chemistry.chemical_compound In vivo medicine Animals Receptor Injections Spinal Acetaminophen Neurotransmitter Agents business.industry General Neuroscience digestive oral and skin physiology Analgesics Non-Narcotic Spinal cord Rats stomatognathic diseases medicine.anatomical_structure Nociception Spinal Cord chemistry Hyperalgesia medicine.symptom business medicine.drug |
| Zdroj: | Neuroscience Letters. 442:50-53 |
| ISSN: | 0304-3940 |
| Popis: | Acetaminophen is an analgesic and antipyretic drug believed to exert its effect through interruption of nociceptive processing. In order to determine whether this effect is due to peripheral or central activity, we studied the efficacy of systemic (oral) and intrathecal (IT) application of acetaminophen in preventing the development of hyperalgesia induced through the direct activation of pro-algogenic spinal receptors. Spinal administration of substance P (SP, 30 nmol, IT) in rats produced a decreased thermal threshold, indicating centrally mediated hyperalgesia. Pretreatment of rats with oral acetaminophen (300 mg/kg), but not vehicle, significantly attenuated IT SP-induced hyperalgesia. Acetaminophen given IT also produced a dose-dependent (10–200 μg) antinociceptive effect. In addition, oral acetaminophen suppressed spinal PGE 2 release evoked by IT SP in an in vivo IT dialysis model. The ability of IT as well as oral acetaminophen to reverse this spinally initiated hyperalgesia emphasizes the likely central action and bioavailability of the systemically delivered drug. Jointly, these data argue for an important central antihyperalgesic action of acetaminophen. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect