Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030201 (Postoperative pain)
 1,085 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Postoperative pain, arising due to surgical tissue injury, is most frequent type of pain found in clinical practice. In postoperative analgesia opioids still constitute the fundamental form of pain treatment, but the development of neurophysiology and neuropharmacology has allowed for the optimization of postoperative analgesia. Therefore, in order to potentialize the pain relief effect of opioids and/or inhibit the nociception process and its consequences, diverse drugs and therapies are used. The procedure is called multimodal analgesia and consists in the administration of opioids in conjunction with NMDA antagonists, COX inhibitors, cholecystokinin antagonists, agonists of muscarine receptors, agonists of alpha-2 receptors or cytokine inhibitors. An alternative or supplementary therapy in the postoperative period relies on local anaesthetic techniques or TENS. There also exists pre-emptive analgesia, whose aim is to safeguard the central nervous system from increased afferent nociceptive stimulation during the operation.
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PMID:[Postoperative pain treatment]. 1096 35

Postoperative pain significantly impacts patient recovery. However, postoperative pain management remains suboptimal, perhaps because treatment strategies are based mainly on studies using inflammatory pain models. We used a recently developed mouse model of incisional pain to investigate peripheral and spinal mechanisms contributing to heat hyperalgesia after incision. Behavioral experiments involving TRPV1 KO mice demonstrate that, as previously observed in inflammatory models, TRPV1 is necessary for heat (but not mechanical) hyperalgesia after incision. However, in WT mice, neither the proportion of TRPV1 immunoreactive neurons in the DRG nor the intensity of TRPV1 staining in the sciatic nerve was different from that in controls up to 4 days after incision. This result was corroborated by immunoblot analysis of sciatic nerve in rats subjected to an incision, and is distinct from that following inflammation of the rat hind paw, a situation in which TRPV1 expression levels in sciatic nerve increases. In the absence of heat exposure, spinal c-Fos staining was similar between incised TRPV1 KO and WT mice. However, differences in c-Fos staining between heat exposed TRPV1 KO and WT mice after incision suggest that the incision-mediated enhancement of heat-evoked signaling to the spinal cord involves a TRPV1-dependent mechanism. Finally, heat hyperalgesia after incision was reversed by antagonism of spinal non-NMDA receptors, unlike inflammatory hyperalgesia, which is mediated via NMDA receptors . Thus, TRPV1 is important for the generation of thermal hyperalgesia after incision. Our observations suggest that all experimental pain models may not be equally appropriate to guide the development of postoperative pain therapies.
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PMID:Heat hyperalgesia after incision requires TRPV1 and is distinct from pure inflammatory pain. 1591 Nov 56