Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Analgesia (NAA) caused by nonacupuncture point (abdominal muscle) stimulation after lesioning the analgesia inhibitory system (AIS) or treating the subject with proglumide was abolished by hypophysectomy or adrenalectomy. The final sector of the NAA afferent pathway from the nonacupuncture point to the pituitary gland and the initial sector of the descending pain inhibitory system were found in the anterior and posterior arcuate nucleus (A-HARN and P-HARN), respectively. Analgesia caused by ACTH microinjected into the P-HARN disappeared after denervation of the A-HARN, but that caused by dopamine did not. Firing rates of P-HARN neurons were increased by nonacupuncture point simulation (NAPS) after lesion of the AIS or treatment with proglumide. The NAPS responsive neurons also responded to ultramicroinjected dopamine, but not to ultramicroinjected ACTH. Both NAA and NAPS responsive neuron activity that were abolished by hypophysectomy were restored by concurrent application of NAPS and intraperitoneal ACTH. Reduction of sodium ions due to adrenalectomy was found to abolish NAA. It was concluded that NAA production involves dopaminergic transmission in the HARN and ACTH acting presynaptically on this transmission.
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PMID:Analgesia produced by pituitary ACTH and dopaminergic transmission in the arcuate. 165 17

Lesion of the preoptic area (POA) or medial arcuate nucleus (M-HARN) abolished acupuncture analgesia (AA). Potentials in the median eminence (ME) evoked by stimulation of the acupuncture point (AP) were not affected by lesion of either the POA or M-HARN alone, but were abolished by concurrent lesion of both. No analgesia was produced by stimulation of the POA. Analgesia produced by stimulation of the M-HARN was abolished by lesion of the POA, and the abolished analgesia was restored by concurrent stimulation of the POA and M-HARN, hence POA and M-HARN outputs might converge in the ME to produce AA. Similar convergence from the anterior arcuate nucleus (A-HARN) and POA to the ME was observed in analgesia (NAA) produced by stimulation of a nonacupuncture point (NAP). Two pathways diverged from the lateral hypothalamus in the AA afferent pathway and two from the lateral periaqueductal central gray (L-PAG) in the NAA afferent pathway. POA potentials evoked by stimulation of the AP were reversed by naloxone, and those evoked by stimulation of the AP were reversed by dexamethasone. ACTH sensitive sites were found in both the L-PAG and the anterior hypothalamus.
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PMID:Convergence from the preoptic area and arcuate nucleus to the median eminence in acupuncture and nonacupuncture point stimulation analgesia. 193 97

Antiserum of methionine-enkephalin (Met-Enk) applied intrathecally abolished acupuncture analgesia (AA) caused by low frequency stimulation of an acupuncture point (tibial muscle, APS) of rats, but antisera of leucine-enkephalin (Leu-Enk) and dynorphin (Dyn) did not. Antiserum of Dyn applied intrathecally abolished analgesia (NAA) produced by stimulation of a nonacupuncture point (NAPS) which was revealed by lesion in the analgesia inhibitory system (AIS), whereas antisera of Met-Enk and Leu-Enk did not. NAA was antagonized by the kappa-receptor antagonist, Mr2266, and analgesia was produced by the kappa-agonist, U50-488H, in the AIS lesioned rats. Potentials in the dorsal periaqueductal central gray (D-PAG) evoked by APS were antagonized by naloxone and antiserum of Met-Enk, and those in the lateral PAG (L-PAG) evoked by NAPS were antagonized by Mr2266 and antiserum of Dyn. After adrenalectomy, AA, potentials in the D-PAG, and analgesia caused by stimulation (SPA) of the D-PAG were abolished 12 hour; and NAA, potentials in the L-PAG, and SPA of the L-PAG were abolished in 24 hour. All were then restored one hour after intravenous application of 1 ml of 5% NaCl solution. AA and NAA which were augmented for several hours before their abolition after adrenalectomy were not antagonized by naloxone nor M 2266, respectively. However naloxone and Mr2266 did antagonize AA and NAA, respectively, one hour after treatment with 1 ml of 5% NaCl solution.
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PMID:Differentiation of acupuncture and nonacupuncture points by difference of associated opioids in the spinal cord in production of analgesia by acupuncture and nonacupuncture point stimulation, and relations between sodium and those opioids. 198 42

The popliteal fossa nerve block (PFNB) offers numerous advantages that make it a suitable anesthetic technique for foot and ankle surgery. In this retrospective study, we investigated the acute and long-term safety and efficacy of this relatively underutilized anesthetic technique for foot and ankle surgery. A review of 834 patients who underwent foot and/or ankle surgery by the coauthor (NAA) was conducted. Four hundred sixty-seven patients received a PFNB with the aid of a peripheral nerve stimulator. Variables assessed included the quality of surgical anesthesia, postoperative analgesia and the acute and long-term incidence of postoperative neuralgia and neuropraxia. The PFNBs were performed by anesthesiologists with various levels of training at a tertiary care hospital and all were supplemented with a saphenous nerve block. The PFNB was successful as the sole anesthetic technique in 79% of the cases; 18% were converted to general anesthesia and 3% required augmentation with local anesthetic. There were no complications associated with the PFNB. There were no incidents of postoperative neuralgia or neuropraxia. Only 12% of patients with a successful block required analgesics in the PACU, while 60% of patients with a failed block required systemic analgesics for surgical site pain (p<0.01). These results suggest that the performance of the PFNB with the guidance of a peripheral nerve stimulator is a safe and effective anesthetic technique for foot and ankle surgery.
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PMID:Safety and efficacy of the popliteal fossa nerve block when utilized for foot and ankle surgery. 1204 82

It was investigated the duration of pain response-licking of a back paw after injection of a solution of formalin (5% on 0.025 ml) in a dorsal surface of a back paw and the level of analgesia evoked by microwaves of low intensity on the point of acupuncture E-36 applied during 10 minutes on injected back paw in mice of genotypes C57B1/6j (C57), CBA/CaLac (CBA) and white laboratory mice. It was shown that the mice C57 had the largest duration of pain response and the lowest level of analgesia (8.3%) when compared with mice CBA and white laboratory mice. The mice of a genotype NAA had the shortest duration of pain response, but an average level of analgesia (13.8%) in comparison with mice C57 and white laboratory mice. The white laboratory mice had average duration of pain response but the greatest level of analgesia (24.2%) in comparison with mice of a genotype C57 and CBA.
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PMID:[Evaluation of analgesia evoked by microwaves of low intensity in the point of acupuncture in mice with different genotypes]. 1517 9

Surgical incision-induced nociception contributes to the occurrence of postoperative cognitive dysfunction. However, the exact mechanisms involved remain unclear. Brain-derived neurotrophic factor (BDNF) has been demonstrated to improve fear learning ability. In addition, BDNF expression is influenced by the peripheral nociceptive stimulation. Therefore, we hypothesized that surgical incision-induced nociception may cause learning impairment by inhibiting the BDNF/tropomyosin-related kinase B (TrkB) signaling pathway. The fear conditioning test, enzyme-linked immunosorbent assay, and Western blot analyses were used to confirm our hypothesis and determine the effect of a plantar incision on the fear learning and the BDNF/TrkB signaling pathway in the hippocampus and amygdala. The freezing times in the context test and the tone test were decreased after the plantar incision. A eutectic mixture of local anesthetics attenuated plantar incision-induced postoperative pain and fear learning impairment. ANA-12, a selective TrkB antagonist, abolished the improvement in fear learning and the activation of the BDNF signaling pathway induced by eutectic mixture of local anesthetics. Based on these results, surgical incision-induced postoperative pain, which was attenuated by postoperative analgesia, caused learning impairment in mice partially by inhibiting the BDNF signaling pathway. These findings provide insights into the mechanism underlying surgical incision-induced postoperative cognitive function impairment.
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PMID:Surgical incision induces learning impairment in mice partially through inhibition of the brain-derived neurotrophic factor signaling pathway in the hippocampus and amygdala. 3023 30