naloxone has been researched along with Acute-Pain* in 21 studies
1 review(s) available for naloxone and Acute-Pain
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Caring for patients with opioid use disorder in the hospital.
Topics: Acute Pain; Analgesics, Non-Narcotic; Analgesics, Opioid; Buprenorphine; Buprenorphine, Naloxone Drug Combination; Drug Overdose; Hospitalization; Humans; Methadone; Naloxone; Narcotic Antagonists; Opiate Substitution Treatment; Opioid-Related Disorders; Respiration, Artificial; Substance Withdrawal Syndrome | 2016 |
2 trial(s) available for naloxone and Acute-Pain
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OPAL: a randomised, placebo-controlled trial of opioid analgesia for the reduction of pain severity in people with acute spinal pain. Trial protocol.
Low back pain and neck pain are extremely prevalent and are responsible for an enormous burden of disease globally. Strong analgesics, such as opioid analgesics, are recommended by clinical guidelines for people with acute low back pain or neck pain who are slow to recover and require more pain relief. Opioid analgesics are widely and increasingly used, but there are no strong efficacy data supporting the use of opioid analgesics for acute low back pain or neck pain. Concerns regarding opioid use are further heightened by the risks of adverse events, some of which can be serious (eg, dependency, misuse and overdose).. OPAL is a randomised, placebo-controlled, triple-blinded trial that will investigate the judicious use of an opioid analgesic in 346 participants with acute low back pain and/or neck pain who are slow to recover. Participants will be recruited from general practice and randomised to receive the opioid analgesic (controlled release oxycodone plus naloxone up to 20 mg per day) or placebo in addition to guideline-based care (eg, reassurance and advice of staying active) for up to 6 weeks. Participants will be followed-up for 3 months for effectiveness outcomes. The primary outcome will be pain severity. Secondary outcomes will include physical functioning and time to recovery. Medication-related adverse events will be assessed and a cost-effectiveness analysis will be conducted. We will additionally assess long-term use and risk of misuse of opioid analgesics for up to 12 months.. Ethical approval has been obtained. Trial results will be disseminated by publications and conference presentations, and via the media.. ACTRN12615000775516: Pre-results. Topics: Acute Pain; Adolescent; Adult; Aged; Analgesics, Opioid; Australia; Cost-Benefit Analysis; Female; Humans; Low Back Pain; Male; Middle Aged; Naloxone; Neck Pain; Oxycodone; Pain Measurement; Research Design; Young Adult | 2016 |
What do plasma beta-endorphin levels reveal about endogenous opioid analgesic function?
Plasma levels of beta-endorphin (BE), an endogenous opioid analgesic, are often reported as they relate to acute and chronic pain outcomes. However, little is known about what resting plasma BE levels might reveal about functioning of the endogenous opioid antinociceptive system. This study directly examined associations between resting plasma BE and subsequent endogenous opioid analgesic responses to acute pain in 39 healthy controls and 37 individuals with chronic low back pain (LBP). Resting baseline levels of plasma BE were assessed. Next, participants received opioid blockade (8 mg naloxone i.v.) or placebo in a double-blind, randomized, crossover design. Participants then underwent two acute pain stimuli: finger pressure (FP) pain and ischaemic (ISC) forearm pain. Blockade effects (naloxone minus placebo pain ratings) were derived to index endogenous opioid analgesic function. In placebo condition analyses for both pain stimuli, higher resting BE levels were associated with subsequently greater reported pain intensity (p's < 0.05), with this effect occurring primarily in healthy controls (BE × Participant Type interactions, p's < 0.05). In blockade effect analyses across both pain tasks, higher resting plasma BE predicted less subsequent endogenous opioid analgesia (smaller blockade effects; p's < 0.05). For the ISC task, these links were significantly more prominent in LBP participants (BE × Participant Type Interactions, p's < 0.05). Results suggest that elevated resting plasma BE may be a potential biomarker for reduced endogenous opioid analgesic capacity, particularly among individuals with chronic pain. Potential clinical implications are discussed. Topics: Acute Pain; Adult; Analgesia; beta-Endorphin; Chronic Pain; Cross-Over Studies; Double-Blind Method; Female; Humans; Low Back Pain; Male; Middle Aged; Naloxone; Narcotic Antagonists; Pain Measurement; Pain Threshold; Physical Stimulation | 2012 |
18 other study(ies) available for naloxone and Acute-Pain
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Antinociceptive Efficacy of the µ-Opioid/Nociceptin Peptide-Based Hybrid KGNOP1 in Inflammatory Pain without Rewarding Effects in Mice: An Experimental Assessment and Molecular Docking.
Topics: Acute Pain; Analgesics; Animals; Behavior, Animal; CHO Cells; Cricetinae; Cricetulus; Cycloheptanes; Humans; Hyperalgesia; In Vitro Techniques; Inflammation; Male; Mice; Models, Molecular; Molecular Docking Simulation; Morphine; Movement; Naloxone; Naltrexone; Nociceptin; Oligopeptides; Opioid Peptides; Pain Management; Piperidines; Receptors, Opioid, mu | 2021 |
The analgesic effect of refeeding on acute and chronic inflammatory pain.
Pain is susceptible to various cognitive factors. Suppression of pain by hunger is well known, but the effect of food intake after fasting (i.e. refeeding) on pain remains unknown. In the present study, we examined whether inflammatory pain behavior is affected by 24 h fasting and 2 h refeeding. In formalin-induced acute inflammatory pain model, fasting suppressed pain behavior only in the second phase and the analgesic effect was also observed after refeeding. Furthermore, in Complete Freund's adjuvant-induced chronic inflammatory pain model, both fasting and refeeding reduced spontaneous pain response. Refeeding with non-calorie agar produced an analgesic effect. Besides, intraperitoneal (i.p.) administration of glucose after fasting, which mimics calorie recovery following refeeding, induced analgesic effect. Administration of opioid receptor antagonist (naloxone, i.p.) and cannabinoid receptor antagonist (SR 141716, i.p.) reversed fasting-induced analgesia, but did not affect refeeding-induced analgesia in acute inflammatory pain model. Taken together, our results show that refeeding produce analgesia in inflammatory pain condition, which is associated with eating behavior and calorie recovery effect. Topics: Acute Pain; Analgesics, Opioid; Animals; Chronic Pain; Disease Models, Animal; Eating; Food Deprivation; Formaldehyde; Freund's Adjuvant; Glucose; Hot Temperature; Hyperalgesia; Inflammation; Injections, Intraperitoneal; Male; Mice; Mice, Inbred C57BL; Naloxone; Narcotic Antagonists; Pain Management; Pain Measurement; Rimonabant | 2019 |
Tapentadol in an Experimental Animal Model of Acute Orofacial Pain.
Tapentadol exhibits a synergistic dual effect effect (MOR / NRI) -agonist effect on noradrena-line reuptake inhibition (NRI). Tapentadol is effective on pain with neuropathic characteristics, therefore we decided to use it in an experimental model of acute orofacial pain.. The Orofacial Stimulation Test, developed by Ugo Basile, measures hypersensitivity to thermal or mechanical stimulation of the trigeminal area. In the experiment, rats had to voluntarily contact a thermal or mechanical stimulator with their unshaved vibrissal pad in order to access a food reward. Twenty adult laboratory rats (average weight 345 grams) were tested. Intraperitoneal tapentadol was used in doses of 1 mg/kg and 2 mg/kg.. The results of the pilot study indicate that intraperitoneal administration of tapentadol (2 mg/kg) increased mechanical anti-nociception in rats. Topics: Acute Pain; Analgesics, Opioid; Animals; Central Amygdaloid Nucleus; Dose-Response Relationship, Drug; Facial Pain; Naloxone; Pain Measurement; Pilot Projects; Rats; Tapentadol; Yohimbine | 2019 |
TRPV1 promotes opioid analgesia during inflammation.
Pain and inflammation are inherently linked responses to injury, infection, or chronic diseases. Given that acute inflammation in humans or mice enhances the analgesic properties of opioids, there is much interest in determining the inflammatory transducers that prime opioid receptor signaling in primary afferent nociceptors. Here, we found that activation of the transient receptor potential vanilloid type 1 (TRPV1) channel stimulated a mitogen-activated protein kinase (MAPK) signaling pathway that was accompanied by the shuttling of the scaffold protein β-arrestin2 to the nucleus. The nuclear translocation of β-arrestin2 in turn prevented its recruitment to the μ-opioid receptor (MOR), the subsequent internalization of agonist-bound MOR, and the suppression of MOR activity that occurs upon receptor desensitization. Using the complete Freund's adjuvant (CFA) inflammatory pain model to examine the role of TRPV1 in regulating endogenous opioid analgesia in mice, we found that naloxone methiodide (Nal-M), a peripherally restricted, nonselective, and competitive opioid receptor antagonist, slowed the recovery from CFA-induced hypersensitivity in wild-type, but not TRPV1-deficient, mice. Furthermore, we showed that inflammation prolonged morphine-induced antinociception in a mouse model of opioid receptor desensitization, a process that depended on TRPV1. Together, our data reveal a TRPV1-mediated signaling pathway that serves as an endogenous pain-resolution mechanism by promoting the nuclear translocation of β-arrestin2 to minimize MOR desensitization. This previously uncharacterized mechanism may underlie the peripheral opioid control of inflammatory pain. Dysregulation of the TRPV1-β-arrestin2 axis may thus contribute to the transition from acute to chronic pain. Topics: Acute Pain; Analgesia; Analgesics, Opioid; Animals; beta-Arrestin 2; Chronic Pain; Disease Models, Animal; Freund's Adjuvant; Humans; Inflammation; Mice; Mice, Knockout; Naloxone; Narcotic Antagonists; Quaternary Ammonium Compounds; Signal Transduction; TRPV Cation Channels | 2019 |
Synthesis of novel norsufentanil analogs via a four-component Ugi reaction and in vivo, docking, and QSAR studies of their analgesic activity.
Novel substituted amino acid tethered norsufentanil derivatives were synthesized by the four-component Ugi reaction. Norsufentanil was reacted with succinic anhydride to produce the corresponding carboxylic acid. The resulting carboxylic acid has undergone a multicomponent reaction with different aldehydes, amines, and isocyanides to produce a library of the desired compounds. In all cases, amide bond rotation was observed in the NMR spectra. In vivo analgesic activity of the synthesized compounds was evaluated by a tail flick test. Very encouraging results were obtained for a number of the synthesized products. Some of the synthesized compounds such as 5a, 5b, 5h, 5j, and 5r were found to be more potent than sufentanil, sufentanil citrate, and norsufentanil. Binding modes between the compounds and mu and delta-opioid receptors were studied by molecular docking method. The relationship between the molecular structural features and the analgesic activity was investigated by a quantitative structure-activity relationship model. The results of the molecular modeling studies and the in vivo analgesic activity suggested that the majority of the synthesized compounds were more potent than sufentanil and norsufentanil. Topics: Acute Pain; Analgesics; Animals; Binding Sites; Male; Mice; Molecular Docking Simulation; Naloxone; Protein Structure, Tertiary; Quantitative Structure-Activity Relationship; Receptors, Opioid, delta; Receptors, Opioid, mu; Sufentanil | 2018 |
Weighing the Risks and Benefits of Chronic Opioid Therapy.
Evidence supports the use of opioids for treating acute pain. However, the evidence is limited for the use of chronic opioid therapy for chronic pain. Furthermore, the risks of chronic therapy are significant and may outweigh any potential benefits. When considering chronic opioid therapy, physicians should weigh the risks against any possible benefits throughout the therapy, including assessing for the risks of opioid misuse, opioid use disorder, and overdose. When initiating opioid therapy, physicians should consider buprenorphine for patients at risk of opioid misuse, opioid use disorder, and overdose. If and when opioid misuse is detected, opioids do not necessarily need to be discontinued, but misuse should be noted on the problem list and interventions should be performed to change the patient's behavior. If aberrant behavior continues, opioid use disorder should be diagnosed and treated accordingly. When patients are discontinuing opioid therapy, the dosage should be decreased slowly, especially in those who have intolerable withdrawal. It is not unreasonable for discontinuation of chronic opioid therapy to take many months. Benzodiazepines should not be coprescribed during chronic opioid therapy or when tapering, because some patients may develop cross-dependence. For patients at risk of overdose, naloxone should be offered to the patient and to others who may be in a position to witness and reverse opioid overdose. Topics: Acute Pain; Analgesics, Opioid; Buprenorphine; Chronic Pain; Drug Overdose; Education, Medical, Continuing; Humans; Male; Naloxone; Opioid-Related Disorders; Practice Guidelines as Topic; Practice Patterns, Physicians'; Risk Assessment; United States | 2016 |
The oral administration of trans-caryophyllene attenuates acute and chronic pain in mice.
Trans-caryophyllene is a sesquiterpene present in many medicinal plants' essential oils, such as Ocimum gratissimum and Cannabis sativa. In this study, we evaluated the antinociceptive activity of trans-caryophyllene in murine models of acute and chronic pain and the involvement of trans-caryophyllene in the opioid and endocannabinoid systems. Acute pain was determined using the hot plate test (thermal nociception) and the formalin test (inflammatory pain). The chronic constriction injury (CCI) of the sciatic nerve induced hypernociception was measured by the hot plate and von Frey tests. To elucidate the mechanism of action, mice were pre-treated with naloxone or AM630 30 min before the trans-caryophyllene treatment. Afterwards, thermal nociception was evaluated. The levels of IL-1β were measured in CCI-mice by ELISA. Trans-caryophyllene administration significantly minimized the pain in both the acute and chronic pain models. The antinociceptive effect observed during the hot plate test was reversed by naloxone and AM630, indicating the participation of both the opioid and endocannabinoid system. Trans-caryophyllene treatment also decreased the IL-1β levels. These results demonstrate that trans-caryophyllene reduced both acute and chronic pain in mice, which may be mediated through the opioid and endocannabinoid systems. Topics: Acute Pain; Administration, Oral; Analgesics; Animals; Cannabis; Chronic Pain; Formaldehyde; Hot Temperature; Hyperalgesia; Inflammation; Interleukin-1beta; Male; Mice; Mice, Inbred C57BL; Naloxone; Ocimum; Oils, Volatile; Phytotherapy; Plant Extracts; Polycyclic Sesquiterpenes; Sesquiterpenes | 2014 |
Antihyperalgesic effects of ginseng total saponins in a rat model of incisional pain.
The aim of this study was to assess whether intraperitoneal administration of ginseng total saponins (GTS) has antihyperalgesic effects in a rat model of incisional pain. The proinflammatory responses and reversal of the antihyperalgesic effect of GTS by N-methyl-d-aspartate (NMDA) or naloxone were also evaluated.. Rats were injected intraperitoneally with 0.9% saline vehicle or various doses of GTS before or after a plantar incision. Paw withdrawal in response to application of the von Frey filament with the lowest bending force marked the mechanical withdrawal threshold (MWT). Blood samples were collected for the assessment of serum interleukin (IL)-1β and IL-6 levels. The IL levels were measured using an enzyme-linked immunosorbent assay kit. Rats were injected intraperitoneally with NMDA or naloxone before the GTS injection to assess the reversal of the antihyperalgesic effect of GTS.. The MWT measured 2 h after the plantar incision increased significantly after the postincision administration of 50, 100, or 200 mg/kg of GTS compared with the MWT at 2 h after plantar incision. The MWT also increased significantly after the preincision injection of 100 or 200 mg/kg of GTS compared with the MWT of the vehicle control. Administration of GTS suppressed the postincision rise in serum IL-1β levels and NMDA inhibited the increase in the MWT compared with GTS alone.. Intraperitoneal administration of GTS before or after surgery induces antihyperalgesic effects in a rat model of incisional pain. The effects on mechanical hyperalgesia may be associated with anti-inflammatory cytokines and NMDA signaling. Topics: Acute Pain; Animals; Disease Models, Animal; Excitatory Amino Acid Agonists; Hyperalgesia; Injections, Intraperitoneal; Male; N-Methylaspartate; Naloxone; Narcotic Antagonists; Pain, Postoperative; Panax; Rats; Rats, Sprague-Dawley; Saponins | 2014 |
Role of GABAA receptor in modulation of acute thermal pain using a rat model of cholestasis.
Increased activity of the endogenous opioid system in cholestasis results in analgesia. GABAA receptors have been ascribed both pronociceptive and antinociceptive roles in pain modulation. Considering the elevated endogenous opioid tone in cholestasis and the existence of close interaction between the GABAergic and opioidergic systems in pain control, the involvement of GABAA receptors in modulation of nociception in a model of elevated endogenous opioid tone, cholestasis, was investigated using muscimol and bicuculline as selective GABAA receptor agonist and antagonist respectively. Cholestasis was induced by ligation of the main bile duct using two ligatures and transsection of the duct between them. Cholestatic rats had increased tail-flick latencies (TFLs) compared to non-cholestatic rats. Administration of muscimol (0.2 and 0.4 mg/kg, s.c.) and bicuculline (0.5 and 1mg/kg, s.c.) to the cholestatic groups significantly increased and decreased respectively TFLs compared to the saline treated cholestatic group. Muscimol antinociception in cholestatic animals was attenuated by co-administration of naloxone or bicuculline. Furthermore, the combination of bicuculline and naloxone completely reversed the increased TFLs of cholestatic rats back to the level of unoperated animals. Muscimol and bicuculline injections into non-cholestatic animals did not alter TFLs. At the doses used here, none of the drugs impaired motor coordination, as revealed by the rotarod test. This study shows the involvement of GABAA receptors in pain modulation during cholestasis in rats. Topics: Acute Pain; Animals; Bicuculline; Cholestasis; Disease Models, Animal; Muscimol; Naloxone; Rats; Receptors, GABA-A; Rotarod Performance Test | 2014 |
ASPMN survey--nurses' practice patterns related to monitoring and preventing respiratory depression.
The American Society for Pain Management Nursing convened a taskforce to develop guidelines on monitoring for opioid-induced sedation and respiratory depression. Part of the guideline development was the determination of nursing practice patterns related to monitoring and preventing respiratory depression during the administration of analgesics for pain. One hundred and forty-seven responses were received from 90 unique institutions across the United States. Monitoring adults with intermittent pulse oximetry while using intravenous patient-controlled analgesia (IV PCA) was 58%. Adults were monitored with continuous pulse oximetry by 25% of respondents. When using continuous epidural analgesia, 56% of patients were monitored intermittently, and 40% were monitored continuously. The use of end tidal CO2 (ETCO2) monitoring was much less, with 2.2% patients on epidural therapy, and 1.5% of institutions were using ETCO2 with IV PCA. The survey also included the location of the alarm, respiratory parameters for alarms, changes in procedures reported by institutions, and definitions of high-risk patients. Topics: Acute Pain; Analgesics, Opioid; Carbon Dioxide; Clinical Alarms; Conscious Sedation; Health Care Surveys; Humans; Monitoring, Physiologic; Naloxone; Narcotic Antagonists; Nursing Staff, Hospital; Oximetry; Practice Guidelines as Topic; Professional Practice; Respiratory Insufficiency; Risk Management; United States | 2013 |
Acute pain control challenges with buprenorphine/naloxone therapy in a patient with compartment syndrome secondary to McArdle's disease: a case report and review.
We report the first case of non-iatrogentic exertional rhabdomyolysis leading to acute compartment syndrome in a patient with McArdle's disease. We describe considerations of concurrent buprenorphine/naloxone therapy during episodes of severe acute pain.. Case report.. A 50-year-old male with a history of McArdle's disease, taking buprenorphine/naloxone for chronic pain and opioid dependence, presented to the Emergency Department with severe bilateral anterior thigh pain. Over the following 8 hours, he was given a total of 12 mg of intravenous hydromorphone with minimal pain relief. The decision was made to initiate patient-controlled analgesia (PCA) with hydromorphone started at 0.5 mg as needed with a 15-minute lockout. Subsequently, the patient's anterior thighs were found to be extremely tense. His creatine kinase level rose to 198,688 units/L and compartment pressures were greater than 90 mm Hg bilaterally. The patient was taken for emergent bilateral fasciotomies. The hydromorphone PCA was increased to 0.8 mg as needed with a 15-minute lockout and a basal rate of 0.5 mg/h. The patient's reported pain plateaued at 3/10 intensity 2 days after surgery, and he was transitioned to oxycodone and hydrocodone/acetaminophen. He followed up with his pain management physician 2 months later who restarted suboxone and a buphrenorphine transdermal patch.. Buprenorphine/naloxone is being prescribed off-label with increasing frequency for pain management in patients with or without a history of opioid abuse. Severe acute pain is more difficult to control with opioid analgesics in patients taking buprenorphine/naloxone, requiring higher than usual doses. If buprenorphine/naloxone is discontinued to better treat acute pain with other opioids, monitoring for overdose must take place for at least 72 hours. Topics: Acetaminophen; Acute Pain; Analgesia, Patient-Controlled; Analgesics, Non-Narcotic; Analgesics, Opioid; Buprenorphine; Compartment Syndromes; Creatine Kinase; Drug Combinations; Glycogen Storage Disease Type V; Humans; Hydromorphone; Injections, Intramuscular; Male; Middle Aged; Naloxone; Narcotic Antagonists; Opioid-Related Disorders; Pain Measurement; Rhabdomyolysis | 2013 |
Novel fentanyl-based dual μ/δ-opioid agonists for the treatment of acute and chronic pain.
Approximately one third of the adult U.S. population suffers from some type of on-going, chronic pain annually, and many more will have some type of acute pain associated with trauma or surgery. First-line therapies for moderate to severe pain include prescriptions for common mu opioid receptor agonists such as morphine and its various derivatives. The epidemic use, misuse and diversion of prescription opioids have highlighted just one of the adverse effects of mu opioid analgesics. Alternative approaches include novel opioids that target delta or kappa opioid receptors, or compounds that interact with two or more of the opioid receptors.. Here we report the pharmacology of a newly synthesized bifunctional opioid agonist (RV-Jim-C3) derived from combined structures of fentanyl and enkephalin in rodents. RV-Jim-C3 has high affinity binding to both mu and delta opioid receptors.. Mice and rats were used to test RV-Jim-C3 in a tailflick test with and without opioid selective antagonist for antinociception. RV-Jim-C3 was tested for anti-inflammatory and antihypersensitivity effects in a model of formalin-induced flinching and spinal nerve ligation. To rule out motor impairment, rotarod was tested in rats.. RV-Jim-C3 demonstrates potent-efficacious activity in several in vivo pain models including inflammatory pain, antihyperalgesia and antiallodynic with no significant motor impairment.. This is the first report of a fentanyl-based structure with delta and mu opioid receptor activity that exhibits outstanding antinociceptive efficacy in neuropathic pain, reducing the propensity of unwanted side effects driven by current therapies that are unifunctional mu opioid agonists. Topics: Acute Pain; Analgesics, Opioid; Animals; Anti-Inflammatory Agents, Non-Steroidal; Chronic Pain; Disease Models, Animal; Dose-Response Relationship, Drug; Drug Evaluation, Preclinical; Enkephalins; Fentanyl; Male; Mice; Mice, Inbred ICR; Naloxone; Naltrexone; Narcotic Antagonists; Rats; Rats, Sprague-Dawley; Receptors, Opioid, delta; Receptors, Opioid, mu | 2013 |
Eugenol reduces acute pain in mice by modulating the glutamatergic and tumor necrosis factor alpha (TNF-α) pathways.
Eugenol is utilized together with zinc oxide in odontological clinical for the cementation of temporary prostheses and the temporary restoration of teeth and cavities. This work explored the antinociceptive effects of the eugenol in different models of acute pain in mice and investigated its possible modulation of the inhibitory (opioid) and excitatory (glutamatergic and pro-inflammatory cytokines) pathways of nociceptive signaling. The administration of eugenol (3-300 mg/kg, p.o., 60 min or i.p., 30 min) inhibited 82 ± 10% and 90 ± 6% of the acetic acid-induced nociception, with ID₅₀ values of 51.3 and 50.2 mg/kg, respectively. In the glutamate test, eugenol (0.3-100 mg/kg, i.p.) reduced the response behavior by 62 ± 5% with an ID₅₀ of 5.6 mg/kg. In addition, the antinociceptive effect of eugenol (10 mg/kg, i.p.) in the glutamate test was prevented by the i.p. treatment for mice with naloxone. The pretreatment of mice with eugenol (10 mg/kg, i.p.) was able to inhibit the nociception induced by the intrathecal (i.t.) injection of glutamate (37 ± 9%), kainic (acid kainite) (41 ± 12%), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) (55 ± 5%), and substance P (SP) (39 ± 8%). Furthermore, eugenol (10 mg/kg, i.p.) also inhibited biting induced by tumor necrosis factor alpha (TNF-α, 65 ± 8%). These results extend our current knowledge of eugenol and confirm that it promotes significant antinociception against different mouse models of acute pain. The mechanism of action appears to involve the modulation of the opioid system and glutamatergic receptors (i.e., kainate and AMPA), and the inhibition of TNF-α. Thus, eugenol could represent an important compound in the treatment for acute pain. Topics: Acute Pain; Analgesics, Opioid; Animals; Anti-Inflammatory Agents, Non-Steroidal; Behavior, Animal; Disease Models, Animal; Dose-Response Relationship, Drug; Eugenol; Excitatory Amino Acid Antagonists; GABAergic Neurons; Hypnotics and Sedatives; Male; Mice; Motor Activity; Naloxone; Narcotic Antagonists; Receptors, Glutamate; Receptors, Kainic Acid; Signal Transduction; Tumor Necrosis Factor-alpha | 2013 |
Antinociceptive effect of Lecythis pisonis Camb. (Lecythidaceae) in models of acute pain in mice.
Lecythis pisonis Camb., also known in Brazil as sapucaia, is used in folk medicine against pruritus, muscle pain and gastric ulcer.. To investigate the antinociceptive effect of ethanol extract from Lecythis pisonis leaves (LPEE), fractions (hexane-LPHF, ether-LPEF and ethyl acetate-LPEAF) and mixture of triterpenes [ursolic and oleanolic acids (MT)] in mice.. LPEE and LPEF were evaluated on the acetic acid induced writhings and formalin, capsaicin and glutamate tests. In addition, MT was investigated on the writhings induced by acetic acid, capsaicin and glutamate tests. In the study of some possible mechanisms involved on the antinociceptive effect of LPEF, it was investigated the participation of opioid system, K+ATP channels and L-arginine-nitric oxide pathway.. LPEE (12.5 and 25 mg/kg, p.o.), LPEF and MT (6.25, 12.5 and 25 mg/kg, p.o.) reduced the writhings in comparison to saline. LPEE (100 mg/kg, p.o.) and LPEF (50 mg/kg, p.o.) were effective in inhibiting both phases of formalin test. In capsaicin test, LPEE (100 and 200 mg/kg, p.o.), LPEF (12.5-50 mg/kg, p.o) and MT (6.25-25 mg/kg, p.o.) showed a significant antinociceptive effect compared to the control. LPEE (25 and 50 mg/kg, p.o.), LPEF (50 and 100 mg/kg, p.o.) and MT (12.5 and 25 mg/kg, p.o.) reduced the glutamate-evoked nociceptive response. Treatment with naloxone, L-arginine and glibenclamide reversed the effect of LPEF in glutamate test.. These results indicate the antinociceptive effect of Lecythis pisonis leaves and suggest that this effect may be related to opioid pathway, K+ATP channels, and L-arginine-nitric oxide modulation. Furthermore, these data support the ethnomedical use of this plant. Topics: Acetic Acid; Acute Pain; Analgesics; Animals; Arginine; Behavior, Animal; Capsaicin; Disease Models, Animal; Formaldehyde; Glutamic Acid; Glyburide; Lecythidaceae; Male; Mice; Naloxone; Narcotic Antagonists; Phytotherapy; Plant Extracts; Plant Leaves | 2013 |
Intraplantar injection of linalool reduces paclitaxel-induced acute pain in mice.
Linalool is the principal component of many essential oils known to possess biological activities. We previously reported that intraplantar injection of linalool reduces the nociceptive response as assayed by the capsaicin test. In this study, we sought to determine whether intraplantar injection of linalool could influence the induction of acute pain (allodynia and hyperalgesia) by paclitaxel in mice. Paclitaxel is widely used in cancer chemotherapy for the treatment of solid tumors, but it sometimes induces moderate to severe acute pain. Paclitaxel administered intraperitoneally as a single dose of 5, 10 or 20 mg/kg produced mechanical allodynia and hyperalgesia in mice. Paclitaxel-induced mechanical allodynia and hyperalgesia began 1 day after administration of paclitaxel and resolved within 7 days. Linalool injected into the hindpaw caused a significant reduction in paclitaxel-induced mechanical allodynia and hyperalgesia. Pretreatment with naloxone hydrochloride, an opioid receptor antagonist, or naloxone methiodide, a peripherally acting µ-opioid receptor-preferring antagonist, significantly reversed linalool-induced antiallodynia and antihyperalgesia. Our results provide evidence for the involvement of peripheral opioids in antiallodynia and antihyperalgesia induced by linalool. These results suggest that activation of peripheral opioid receptors may play an important role in reducing paclitaxel-induced mechanical allodynia and hyperalgesia. Topics: Acute Pain; Acyclic Monoterpenes; Animals; Antineoplastic Agents, Phytogenic; Drosophila Proteins; Hyperalgesia; Injections; Male; Mice; Monoterpenes; Naloxone; Narcotic Antagonists; Paclitaxel; Protein Serine-Threonine Kinases | 2012 |
Antinociceptive activity of (-)-(2S,6S)-(6-ethyl-tetrahydropyran-2-yl)-formic acid on acute pain in mice.
Pain is a major cause of distress, both physical and psychological. There is a continuous search for new pharmacologically active analgesic agents with minor adverse effects. Recently, the synthesis of (-)-(2S,6S)-(6-ethyl-tetrahydropyran-2-yl)-formic acid [tetrahydropyran derivative (TD)] was described. The objective of this study was to investigate antinociceptive effects of TD. Its activity was compared with the activity of morphine. The effects of TD and morphine were evaluated in models of inflammatory and noninflammatory pain. TD (6-1200 μmol/kg, intraperitoneally) significantly reduced the nociceptive effects induced by acetic acid or formalin in mice. TD also demonstrated an antinociceptive effect in the tail-flick and hot-plate model. The opioid receptor antagonist, naloxone (at 15 μmol/kg, intraperitoneally), reversed the antinociceptive activity of TD in all the models evaluated. Morphine and TD induced tolerance in mice. However, the onset of tolerance to TD was delayed compared with that induced by morphine. These results indicate that TD develops significant antinociceptive activity and, at least part of its effects seems to be mediated by the opioid system. Topics: Acute Pain; Analgesics; Analgesics, Opioid; Animals; Disease Models, Animal; Dose-Response Relationship, Drug; Drug Tolerance; Formates; Male; Mice; Morphine; Naloxone; Narcotic Antagonists; Pyrans | 2011 |
Central administration of neuronostatin induces antinociception in mice.
Neuronostatin, a recently discovered endogenous bioactive peptide, was encoded by pro-mRNA of somatostatin that contributes to modulation of nociception. However, nociceptive effect of neuronostatin is still not fully known. The aim of this study was to evaluate effect of neuronostatin on nociception and elucidate its possible mechanism of action. Intracerebroventricular (i.c.v.) administration of neuronostatin (0.3, 3, 6, 12nmol/mouse) produced a dose- and time-related antinociceptive effect in the tail immersion assay in mice, an acute pain model. The antinociceptive effect of neuronostatin was significantly antagonized by naloxone, and was strongly inhibited by co-injection with β-funaltrexamine or nor-binaltorphimine, but not by naltrindole. Also, melanocortin 3/4 receptor antagonist, SHU9119, completely blocked the effect of neuronostatin. These data indicated the involvement of both μ- and κ-opioid receptors and central melanocortin system in the analgesic response induced by neuronostatin. In addition, neuronostatin (6nmol, i.c.v.) increased c-Fos protein expression in the periaqueductal gray (PAG) and the nucleus raphe magnus (NRM) that have a pivotal role in regulating descending pain pathways. Taken together, this study is the first to reveal that neuronostatin produces antinociceptive effect via opioid and central melanocortin systems, which is associated with an increase in neuronal activity the PAG and NRM. Topics: Acute Pain; Analgesics; Animals; Dose-Response Relationship, Drug; Immunohistochemistry; Infusions, Intraventricular; Male; Melanocyte-Stimulating Hormones; Mice; Models, Animal; Naloxone; Naltrexone; Narcotic Antagonists; Nociception; Peptide Hormones; Periaqueductal Gray; Proto-Oncogene Proteins c-fos; Receptor, Melanocortin, Type 3; Receptor, Melanocortin, Type 4 | 2011 |
Differential effects of nociceptin/orphanin FQ (NOP) receptor agonists in acute versus chronic pain: studies with bifunctional NOP/μ receptor agonists in the sciatic nerve ligation chronic pain model in mice.
1-(1-Cyclooctylpiperidin-4-yl)-indolin-2-one (SR14150) and 1-(1-(2,3,3a,4,5,6-hexahydro-1H-phenalen-1-yl)piperidinl-4-yl)-indolin-2-one (SR16835) are moderately selective nociceptin/orphanin FQ (NOP) receptor agonists. In the [(35)S]guanosine 5'-O-(3-thiotriphosphate) assay in vitro, SR14150 is a partial agonist at both the NOP and μ-opioid receptors, whereas SR16835 is a full agonist at the NOP receptor and has low efficacy at μ receptors. These compounds were tested for antinociceptive and antiallodynic activity, using mice in chronic pain, subsequent to spinal nerve ligation (SNL) surgery. When administered subcutaneously to mice after SNL surgery, SR14150 but not SR16835 increased tail-flick latency, which was blocked by the opioid antagonist naloxone, but not by the NOP receptor antagonist (-)-cis-1-methyl-7-[[4-(2,6-dichlorophenyl)piperidin-1-yl]methyl]-6,7,8,9-tetrahydro-5H-benzocyclohepten-5-ol (SB-612111). In contrast, both SR14150 and SR16835 had antiallodynic activity when mechanical allodynia was measured with von Frey monofilaments. This effect was completely blocked by SB-612111 but not by naloxone. On the other hand, morphine antinociception and antiallodynia were both blocked by naloxone and potentiated by SB-612111. These results indicate that, in mice, circuitry mediating antinociceptive activity in acute and chronic pain states is different. It is possible that during a chronic pain state, an up-regulated NOP system in the spinal cord leads to NOP receptor-mediated antiallodynia, which is blocked by NOP antagonists. However, supraspinal up-regulation could lead to an attenuation of morphine antinociception and antiallodynia, which can be alleviated by an NOP receptor antagonist. Thus, although neither NOP agonists nor antagonists are effective as analgesics in acute pain, they may have efficacy as analgesics, either alone or in combination with morphine, for treatment of chronic pain. Topics: Acute Pain; Animals; Chronic Pain; Cycloheptanes; Hot Temperature; Hyperalgesia; Indoles; Ligation; Male; Mice; Mice, Inbred ICR; Morphine; Naloxone; Narcotic Antagonists; Nociceptin Receptor; Piperidines; Receptors, Opioid; Sciatic Nerve | 2011 |