Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The serotonergic system is involved in pain transmission and the 5-hydroxytryptamine (5-HT3) receptor subtype mediates some of these effects at the spinal level. Therefore, we explored the effects of the serotonergic system on nifedipine-induced analgesia by using the 5-HT3 receptor antagonist ondansetron. Male Sprague-Dawley rats were pretreated with ondansetron (1 mg/ kg intraperitoneally) or normal saline. After 15 min, rats received injections of nifedipine (15 mg/kg intraperitoneally) or dimethylsulfoxide (DMSO), solvent for nifedipine, as a control. Nociception was assessed by tail-flick method. Rats treated with nifedipine alone had an increase in tail-flick latency of 122%, as measured by the area under the curve, compared to rats treated with DMSO alone. Pretreatment with ondansetron, however completely blocked the analgesic effect of nifedipine, with tail-flick latency remaining at baseline throughout the measurement period. These results indicate that the 5-HT3 receptor plays an important role in the analgesic response to nifedipine and that medications that block this receptor may decrease the analgesic effectiveness of this type of therapy.
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PMID:Ondansetron blocks nifedipine-induced analgesia in rats. 862 50

Acute Reflex Sympathetic Dystrophy (acute RSD) was defined using a reproducible classification. Elevated temperature of the affected extremity ("calor"), measured by the dorsal side of the observer's hand and mentioned by the patient, pain ("dolor") measured by the Visual Analogue Scale (VAS), redness ("rubor"), edema ("tumor") and limited active range of motion ("functio laesa"), all contributed to the classification system. Patients scoring 4 to 5 positive symptoms were considered to have acute RSD. A prospective, randomized and double blind study was performed in 32 patients, all suffering from acute RSD. In all of these patients the primary injury was the result of a previous accident. One patient was taken out of the study because of his surgery. The study involved treatment with a fatty cream with 50% dimethyl sulfoxide (DMSO, group A), or without DMSO (placebo, group B), both for 2 months. All patients received physiotherapy applied within pain limits. Application of the creams resulted in both groups in an improvement of RSD-scores and VAS-scores after 2 months. However, the improvement of the RSD score in patients of group A (DMSO-group) was significantly (P < 0.01) better compared to group B. The results suggest a certain activity of DMSO 50% cream in patients suffering from RSD and is, therefore, recommendable.
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PMID:Treatment of acute reflex sympathetic dystrophy with DMSO 50% in a fatty cream. 872 69

A prospective and randomized trial that compares Jelonet (Smith & Nephew PLC, London, England) with a new hydrocolloid dressing, Dermasorb (Convatec Ltd., Clwyd, United Kingdom), is presented. The dressings were applied on contiguous donor sites in 21 patients that required skin grafting for burn wounds. Pain experienced with the dressing in situ was assessed on days 2, 4, 7, and on two subsequent occasions. During dressing changes, pain experienced was again assessed, bacteriologic swabs were taken, and the percentage of epithelialization was recorded. Questionnaires completed by investigators and patients were used to assess the perceived performances of both dressings. The results showed that Dermasorb is a less painful dressing than Jelonet, in which wounds heal faster. Dermasorb was preferred by both investigators and patients. No clinical or laboratory evidence of any differences of colonization or infection were found. All results were statistically significant. We would strongly recommend the use of Dermasorb as a split-thickness skin graft donor site dressing for a patient with burns.
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PMID:Dermasorb versus Jelonet in patients with burns skin graft donor sites. 873 72

Since there is growing evidence that nerve growth factor (NGF) acts as a mediator of persistent pain states, here we have studied its acute effects on the properties of primary afferent neurones innervating adult rat urinary bladder. Single A delta and C fibres were dissected from the L6 or S1 dorsal roots of urethane anaesthetized rats. The stimulus-response function of these afferents was evaluated with a series of isotonic distensions of the bladder (0-60 cm H2O). The afferents were then studied after filling the bladder with a vehicle solution of 10% DMSO for 30 min, and then again after filling the bladder with a 10 micrograms/ml solution of human recombinant NGF in 10% DMSO. In the control state, and after filling with 10% DMSO, the myelinated and about one-half of the unmyelinated afferents were mechanosensitive with pressure thresholds in the innocuous range and responsiveness extending into the supra physiological, presumed noxious range. The remaining one-half of unmyelinated afferents showed no mechanosensitivity. After filling with NGF, the large majority of units, both myelinated and unmyelinated, sensitised, evidenced by the development of ongoing activity and a leftward shift of stimulus-response functions. Some of the initially nonmechanosensitive units developed a novel mechanosensitivity. The sensitisation began within 30 min of exposure to NGF, and persisted for the period studied (up to the 3 h). In separate experiments, intravesical NGF at concentrations greater than 1 microgram/ml was found to elicit a dose-dependent extravasation of Evan's blue into the bladder. These data support the notion that NGF may be an endogenous mediator in some persistent pain states.
Pain 1996 Jul
PMID:Sensitisation of visceral afferents by nerve growth factor in the adult rat. 885 35

Antinociceptive effect of nifedipine (15 mg/kg i.p.) and verapamil (10 mg/kg s.c.) was examined in rats chronically exposed to nicotine (6 mg/kg/day via Alzet osmotic pump for 28 days) and after nicotine withdrawal. Sham operated rats served as control for testing DMSO (dimethylsulfoxide, a solvent for nifedipine), nifedipine and verapamil alone. Nociception was measured by the tail-flick technique. Nifedipine, but not verapamil, injected to control rats produced a ceiling tail-flick latency (20 sec) 30 min after the injection, lasting for 10 min. In rats exposed to chronic nicotine for 3 days, nifedipine treatment exhibited ceiling tail-flick latency within 10 min lasting for 80 min. Tested in rats exposed to nicotine for 3 weeks, nifedipine treatment produced this effect 25 min after the injection lasting for 60 min. Nicotine withdrawal abolished this effect. Verapamil did not exhibit any significant changes in tail-flick latencies. These data support our hypothesis that smoking patients treated with nifedipine could be at a potential risk in developing a high pain threshold and missing the first sign of heart attack--a chest pain.
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PMID:Antinociceptive effect of nifedipine and verapamil tested on rats chronically exposed to nicotine and after its withdrawal. 912 20

The purpose of this review was to identify and analyze the controlled clinical trial data for peripheral neuropathic pain (PNP) and complex regional pain syndromes (CRPS). A total of 72 articles were found, which included 92 controlled drug trials using 48 different treatments. The methods of these studies were critically reviewed and the results summarized and compared. The PNP trial literature gave consistent support (two or more trials) for the analgesic effectiveness of tricyclic antidepressants, intravenous and topical lidocaine, intravenous ketamine, carbamazepine and topical aspirin. There was limited support (one trial) for the analgesic effectiveness of oral, topical and epidural clonidine and for subcutaneous ketamine. The trial data were contradictory for mexiletine, phenytoin, topical capsaicin, oral non-steroidal anti-inflammatory medication, and intravenous morphine. Analysis of the trial methods indicated that mexiletine and intravenous morphine were probably effective analgesics for PNP, while non-steroidals were probably ineffective. Codeine, magnesium chloride, propranolol, lorazepam, and intravenous phentolamine all failed to provide analgesia in single trials. There were no long-term data supporting the analgesic effectiveness of any drug and the etiology of the neuropathy did not predict treatment outcome. Review of the controlled trial literature for CRPS identified several potential problems with current clinical practices. The trial data only gave consistent support for analgesia with corticosteroids, which had long-term effectiveness. There was limited support for the analgesic effectiveness of topical dimethylsulfoxyde (DMSO), epidural clonidine and intravenous regional blocks (IVRBs) with bretylium and ketanserin. The trial data were contradictory for intranasal calcitonin and intravenous phentolamine and analysis of the trial methods indicated that both treatments were probably ineffective for most patients. There were consistent trial data indicating that guanethidine and reserpine IVRBs were ineffective, and limited trial data indicating that droperidol and atropine IVRBs were ineffective. No placebo controlled data were available to evaluated sympathetic ganglion blocks (SGBs) with local anesthetics, surgical sympathectomy, or physical therapy. Only the capsaicin trials presented data which allowed for meta-analysis. This meta-analysis demonstrated a significant capsaicin effect with a pooled odds ratio of 2.35 (95% confidence intervals 1.48, 3.22). The methods scores were higher (P < 0.01) for the PNP trials (66.2 +/- 1.5, n = 66) than the CRPS trials (57.6 +/- 2.9, n = 26). The CRPS trials tended to use less subjects and were less likely to use placebo controls, double-blinding, or perform statistical tests for differences in outcome measures between groups. There was almost no overlap in the controlled trial literature between treatments for PNP and CRPS, and treatments used in both conditions (intravenous phentolamine and epidural clonidine) had similar results.
Pain 1997 Nov
PMID:A critical review of controlled clinical trials for peripheral neuropathic pain and complex regional pain syndromes. 1006 78

Clinical studies of topical therapy against Herpes simplex virus (HSV) infections have been reviewed. Idoxuridine (IDU) 15% in dimethyl sulfoxide (DMSO), interferons, and penciclovir result in significant clinical benefit against this virus. IDU reduced pain duration and decreased time to loss of crust in a study of 301 patients. Alpha-interferon has shown synergism with other anti-HSV drugs such as caffeine, trifluorothymidine (TFT), DMSO, and nonoxynol-9. Finally, in a study of over 2,000 patients, application of penciclovir cream, both early and late in the course of HSV infection, decreased the duration of lesions, pain, and viral shedding. Acyclovir (ACV)-resistant strains of HSV are susceptible to (S)-1-(3-hydroxy-2-phosphonylmethoxypropyl) cytosine (HPMPC), and ascorbic acid shows promising effects against HSV. Using a vehicle that enhances skin penetration of a drug or possibly further exploring combination therapy may result in efficacious treatment of HSV. The possibility of topical vaccination or topical gene therapy may also prove beneficial in the future.
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PMID:Treatment of Herpes simplex virus infections with topical antiviral agents. 968 81

The possible role of spinal prostanoids in the tactile allodynia and thermal hyperalgesia associated with an experimental model of neuropathic pain was investigated. Neuropathic pain was induced by tight ligation of the L5 and L6 spinal nerves. Tactile allodynia was assessed 7 days after the surgery by measuring hindpaw withdrawal threshold to probing with von Frey filaments. Thermal hyperalgesia and nociception were determined by the 52 degrees C warm-water tail-flick test and by applying radiant heat to the plantar aspect of the hindpaw ipsilateral to the ligation. Minimal antiallodynic effect was produced by intrathecal (i.th.) administration of ketorolac or morphine up to the highest testable dose (100 microg) or by the (R)- or (S)-enantiomers of ketorolac (up to 6 microg) when administered alone. However, i.th. administration of a fixed ratio (1:1) of morphine plus racemic ketorolac or of morphine plus the (S)-enantiomer of ketorolac (S-ketorolac) produced a dose- and time-related antiallodynic effect: ED50 114 +/- 35.9 microg (total dose) for morphine plus ketorolac and 70.5 +/- 21.0 microg (total dose) for morphine plus S-ketorolac. The combination of i.th. morphine plus the (R)-enantiomer of ketorolac (R-ketorolac) (up to 200 microg total dose) was without effect. Similar antiallodynic activity was obtained for the co-administration of i.th. morphine and intravenous (i.v.) racemic ketorolac. In order to investigate the role of cyclooxygenase (COX) isozymes, relatively selective COX1 (piroxicam) and COX2 N-[2-cyclohexyloxy-4-nitrophenyl] metanesulfonamide (NS-398) inhibitors were administered i.th. (60 microg) alone or together with i.th. morphine. Piroxicam, NS-398, morphine and vehicle (90% DMSO) were without significant antiallodynic effect when administered alone, but moderate antiallodynic effects were produced by i.th. administration of fixed ratio (1:1) combinations of morphine with 60 microg each (highest soluble dose) of piroxicam (%MPE = 40.8 +/- 10.2) or NS-398 (%MPE = 32.4 +/- 9.5). Further, the combined i.th. administration of morphine, piroxicam and NS-398 in fixed 1:1:1 ratio (60 microg each) resulted in a supraadditive antiallodynic effect (%MPE = 70.4 +/- 10.8). Finally, morphine, but not ketorolac, given i.th. produced dose-dependent anti nociception in either the tail-flick or the paw-flick tests. However, there was no synergy between morphine and ketorolac against thermal nociception in either of the tests. These findings suggest that spinal prostanoids produced via both COX1 and COX2 pathways may play a role in neuropathic pain states and suggest the clinical utility of opioid plus COX-inhibitor combination therapy.
Pain 1999 Jul
PMID:Synergistic antiallodynic effects of spinal morphine with ketorolac and selective COX1- and COX2-inhibitors in nerve-injured rats. 1042 61

Topical drugs avoid many of the problematic side effects of systemic agents. Immersion of the tail of a mouse into a solution of dimethyl sulfoxide (DMSO)-containing morphine produces a dose-dependent, naloxone-sensitive, analgesia (ED(50) 6.1 mM; CL 4.3, 8.4) limited to the portion of the tail exposed to the drug. DMSO alone in this paradigm had no analgesic activity. Like morphine, the opioids levorphanol (ED(50) 5.0 mM; CL 3.8, 7.8) and buprenorphine (ED(50) 1. 1 mM; CL 0.7, 1.5) were effective topical analgesics. Lidocaine also was active in the tail-flick assay (ED(50) 2.5 mM; CL 2.0, 3.4), with a potency greater than morphine. As expected, the free base of lidocaine was more potent than its salt. Combinations of a low dose of lidocaine with a low dose of an opioid yielded significantly greater than additive effects for all opioids tested. Isobolographic analysis confirmed the presence of synergy between lidocaine and morphine, levorphanol and buprenorphine. These studies demonstrate a potent interaction peripherally between opioids and a local anesthetic and offer potential advantages in the clinical management of pain.
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PMID:Analgesic synergy between topical lidocaine and topical opioids. 1104 87

Interstitial cystitis (IC) is a painful, sterile, disorder of the urinary bladder characterised by urgency, frequency, nocturia and pain. IC occurs primarily in women but also in men with recent findings indicating that chronic, abacterial prostatitis may be a variant of this condition. The prevalence of IC has ranged from about 8 - 60 cases/100,000 female patients depending on the population evaluated. About 10% of patients have severe symptoms that are associated with Hunner's ulcers on bladder biopsy; the rest could be grouped in those with or without bladder inflammation. Symptoms of IC are exacerbated by stress, certain foods and ovulatory hormones. Many patients also experience allergies, irritable bowel syndrome (IBS) and migraines. There have been various reports indicating dysfunction of the bladder glycosaminoglycan (GAG) protective layer and many publications showing a high number of activated bladder mast cells. Increasing evidence suggests that neurogenic inflammation and/or neuropathic pain is a major component of IC pathophysiology. Approved treatments so far include intravesical administration of dimethylsulphoxide (DMSO) or oral pentosanpolysulphate (PPS). New treatments focus on the combined use of drugs that modulate bladder sensory nerve stimulation (neurolytic agents), inhibit neurogenic activation of mast cells, or provide urothelial cytoprotection, together with new drugs with anti-inflammatory activity.
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PMID:New agents for the medical treatment of interstitial cystitis. 1122 50


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