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)

1. Porphyromonas gingivalis is one of the bacteria likely to be related to pain in periodontitis. Several enzymes isolated from P. gingivalis have been reported to have kininogenase activity. Since kinin release could be held responsible for inflammatory symptoms and pain in periodontitis, we investigated whether the inflammatory and algesic effects of a sonic extract from P. gingivalis (PGSE) could be inhibited by the potent bradykinin B2 receptor antagonist, icatibant (Hoe 140). 2. In anaesthetized rats, the subplantar injection of PGSE (0.1 and 1.0 mg) caused a dose-dependent oedema of the hind paws. The net increase of the paw volume 60 min after the injection was 23 +/- 5% and 77 +/- 12%, respectively. The oedema was rich in plasma proteins as determined by the Evans blue method. Pretreatment with icatibant (300 nmol kg-1, s.c.) significantly reduced the effect of 1.0 mg of PGSE whereas the effects of 0.1 mg of PGSE remained unaffected. 3. The subplantar injection of 1.0 mg of PGSE in unanaesthetized rats caused nociceptive behavioural responses which started about 5 min after the injection and lasted for about 10-15 min. These responses were completely prevented by pretreatment with icatibant (300 nmol kg-1, s.c.). 4. The present results show that the plasma extravasation induced by non-algesic doses of a sonic extract from P. gingivalis are caused by mechanisms other than B2 kinin receptor activation whereas inflammatory effects of algesic doses are due to the action of kinins. The pain elicited by the extract is solely mediated by kinins and can be prevented by icatibant. The bradykinin antagonist could thus have a potential for a clinical use against pain associated with periodontal inflammation.
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PMID:Anti-inflammatory and analgesic activity of the bradykinin antagonist, icatibant (Hoe 140), against an extract from Porphyromonas gingivalis. 795 58

To investigate whether progesterone metabolites' antinociceptive effects correlate with their previously established binding efficacies at the GABA receptor complex (GBR), seven progestin metabolites were administered to ovariectomized Long-Evans rats s.c. (Expt. 1), via i.c.v. implantation (Expt. 2) and then i.c.v. infusion (Expt. 3). Progestins, listed from most to least efficacious at the GBR, were THP [5 alpha-pregnan-3 alpha-ol-20-one], THDOC [5 alpha-pregnan-3 alpha,21-diol-20-one], P [4-pregnen-3,20-dione], DHP [5 alpha-pregnan-3,20-dione],17-OH-P [17-hydroxyprogesterone], DHEAS [5-androsten-3 beta-ol-17-one sulfate] and PS [5-pregnen-3 beta-ol-20-one sulfate]. Pain sensitivity was measured via the radiant heat tailflick method 0, 5, 20, 40, 60, 80, 100 and 120 min after weekly progestin administration. Peripheral administration of 0.0, 0.1, 0.4, 1.6, 3.2 or 6.4 mg/kg of potent to moderate agonists of the GBR (THP, THDOC, P and DHP) tended to elevate tailflick latencies above baseline, whereas administration of the non-5 alpha-reduced metabolite (17-OH-P) and GBR antagonists (DHEAS and PS) did not. Intracerebroventricular implantation and infusion (0.0, 0.5, 1.0, 2.0 micrograms/rat) of THP, THDOC, P and DHP all significantly increased tailflick latencies above baseline and vehicle control, consistent with their GBR efficacies. Central 17-OH-P, DHEAS and PS did not elevate tailflick latencies. These rapid differences were unlikely confounded by stress given that corticosterone levels were not elevated (Expt. 4). As pain sensitivity was attenuated rapidly (0-5 min post-i.c.v.) and consistent with GBR efficacies, this suggests that progestins' modulation of pain may occur via GBR action.
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PMID:Progesterone metabolites, effective at the GABAA receptor complex, attenuate pain sensitivity in rats. 803 14

Effects of estrous cycle and acute and chronic access to palatable fluids on tail-flick latency and opiate-induced analgesia were assessed in 124 female Long Evans rats. Following three consistent cycles, rats were water deprived for 8 h and then given ad lib access to 20 ml of either water, a 32% sucrose solution, or corn oil for 5 h. Nociceptive testing was conducted immediately preceding and 30, 60, and 90 min following an SC injection of morphine sulfate (7.5 mg/kg). Diestrus rats had prolonged premorphine tail-flick latencies compared to rats in proestrus. Rats that consumed corn oil had longer tail-flick latencies preceding and 30 min following morphine injections than rats that drank water or the sucrose solution. Rats were retested after they had ad lib access to the same fluid for 3 weeks. No estrous cycle differences were noted following chronic consumption. Rats with chronic access to sucrose showed increased baseline pain sensitivity and increased morphine-induced analgesia at 30, 60, and 90 min postinjection. These data support the notion that palatable fluid consumption attenuates estrous cycle-dependent differences in pain sensitivity.
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PMID:Diet and estrous cycle influence pain sensitivity in rats. 851 68

Ultrasonic vocalizations may be an expression of the affective pain response in laboratory animals. The present experiment compares the effects of morphine to the delta agonist, DPDPE (D-Pen2,D-Pen5 enkephalin) on a range of reflexive, behavioral and affective responses during an aggressive interaction. In experiment 1, naive female Long-Evans rats received morphine (0, 1, 3, 6, 10 micrograms ICV), or DPDPE (0, 30, 60, 100 micrograms ICV). In experiment 2, female rats were treated with naltrindole (1.0 mg/kg IP) 20 min before DPDPE (0, 60, 100 micrograms ICV). The following endpoints were measured: (1) latency to tail flick in response to heat stimuli; (2) high (33-65 kHz) and low (20-32 kHz) frequency ultrasonic and audible vocalizations; (3) defensive behavior; and (4) motoric activity. Following a brief exposure to attack, rats were threatened by the aggressor but protected from further attack by a large, wire mesh cage, thereby allowing for continued behavioral and vocal measurement without the risk of physical injury; video and audio recordings were made during the attack and then during a portion of the protected encounter (2 min). Morphine suppressed pain reactions varying in complexity from a spinal reflex, to an organized escape reaction, to an affective vocal response. The delta agonist, DPDPE, attenuated high frequency ultrasonic calling and tail flick responding. Defensive behaviors were also modulated by DPDPE at doses that had no effect on walking or rearing, indicating behavioral specificity. By contrast, doses of morphine that decreased defensive upright and escape also decreased motor activity. In female rats, morphine and DPDPE share a common profile of effects on a range of functional end-points, but DPDPE appears to modulate more selectively the reactions related to aversiveness without exerting sedative effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Delta opioid receptors: reflexive, defensive and vocal affective responses in female rats. 854 26

Previous research indicates that the paraventricular nucleus of the hypothalamus (PVN) plays an important role in the development of stress-induced analgesia (SIA). Research implicating the PVN in SIA has generally employed the cold-water swim as the stressor and a phasic pain test, such as the tail-flick test, as the pain model. The present study, using the formalin test for tonic pain, investigated the effect of PVN lesions on (1) tonic pain responses and (2) SIA caused by 30 min of restraint. Male Long-Evans rats were randomly assigned to one of four groups. Two groups received electrolytic lesions of the PVN and two additional groups served as sham-operated controls. One group which received PVN lesions and one group which was sham-operated were exposed to 30 min of restraint immediately prior to a 0.05-ml injection of 2.5% formalin into the planter surface of one hindpaw. The remaining groups which either received PVN lesions or were sham-operated received the formalin injection without prior exposure to restraint. During the first phase of the formalin response, PVN lesions did not alter duration of paw elevation scores, but significantly increased duration of paw licking scores. A 30-min period of restraint had no effect on duration of paw elevation scores, but significantly decreased duration of paw licking scores. PVN lesions did not alter the significant decrease in paw licking scores as a result of restraint. During the second phase of the formalin response, PVN lesions did not alter either the duration of paw elevation scores or the duration of paw licking scores. A 30-min period of restraint significantly decreased duration of paw elevation scores, but had no effect on duration of paw licking scores. PVN lesions did not alter the significant decrease in paw elevation scores as a result of restraint. The results indicate that PVN lesions increase paw licking only during the first phase of the formalin response, with no other alterations in paw licking or duration of paw elevation. In addition, a 30-min period of restraint can produce short-term and long-term SIA for tonic pain. The short-term SIA is reflected as a decrease in paw licking, whereas the long-term SIA is reflected as a decrease in paw elevation. In addition, PVN lesions failed to alter SIA during both phases of the formalin test. The differential effect of restraint on pain responses during the two phases of the formalin test and the lack of effect of PVN lesions on SIA for tonic pain suggest that stress engages multiple endogenous pain inhibitory systems.
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PMID:Restraint reduces formalin-test pain but the effect is not influenced by lesions of the hypothalamic paraventricular nucleus. 865 32

We treated 19 patients for chronic ankle instability with a modified Evans procedure. All patients were evaluated after an average follow up of 128 months with detailed questionnaire, clinical examination, and stress radiographs. Although the subjective results were reported as 8 excellent, 7 good, and 4 fair, residual pain was reported by 11 patients. There was a significantly increased number of osteophytes in the treated ankle joint. Stress radiographs demonstrated significantly improved stability in the operated ankle joint. Range of motion was significantly reduced in hindfoot inversion. The results showed that the modified Evans procedure achieved sufficient joint stability at the expense of inversion range of motion. This reconstruction method apparently did not prevent the development of arthrosis.
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PMID:Long-term results of the modified Evans repair for chronic ankle instability. 872 39

This study was designed to investigate neural mechanisms of referred pain in lumbar intervertebral disc lesions. Patients with a degenerative disc in lower lumbar segments occasionally complain of groin pain, which cannot be explained anatomically as having a radicular origin. In rats pretreated with intravenous application of Evans blue dye, the dye extravasation appeared in the groin skin after application of capsaicin to the ventral portion of the L5-6 intervertebral disc. This response occurred even in rats with a sectioned L-5 spinal nerve and sympathetic trunks, but did not occur in rats with a sectioned genitofemoral nerve. Capsaicin topically applied to the sciatic nerve did not cause dye extravasation in the hindpaw. Therefore, groin dye extravasation was not due to a direct effect of capsaicin but, rather, presumably was caused by an "antidromic axon reflex" of dichotomizing C fibers or to a segmental sympathetic reflex causing vascular permeability. The present results indicate that the ventral portion of the lumbar discs is neurally connected to the groin skin via the upper (L-2) lumbar spinal nerves in rats. Groin pain coincident with low-back pain may be explained as referred pain, indicating that a lesion is present in the ventral portion of the lumbar intervertebral disc space.
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PMID:Neural connection between the ventral portion of the lumbar intervertebral disc and the groin skin. 875 63

Progesterone (P), its metabolites, and other neuroactive steroids alter pain thresholds consistent with their efficacies at modulating gamma-aminobutyric acid (GABAA) receptor complexes. We investigated whether estradiol benzoate (EB) potentiates low dosages of neuroactive steroids' effects on pain. Subcutaneous EB (10 micrograms) or sesame oil vehicle was administered to ovariectomized Long-Evans rats (n = 40) 48 h before intracerebroventricular (ICV) infusion of a neuroactive steroid (0.0, 0.1, 0.3, or 0.5 micrograms) in cyclodextrin vehicle. Neuroactive steroids (listed from greatest to least efficacious at GABAA receptor complexes) were THP [5 alpha-pregnan-3 alpha-ol-20-one], THDOC [5 alpha-pregnan-3 alpha, 21-diol-20-one], DHP [5 alpha-pregnan-3,20-dione], P [4-pregnen-3,20-dione], and DHEAS [5-androsten-3 beta-ol-17-one sulfate]. Pain sensitivity was assessed using the radiant heat tail-flick method before and 20 and 60 min following infusion. Estradiol benzoate interacted with the neuroactive steroids to alter tail-flick latencies. In particular, EB potentiated the antinociceptive effect of THP and DHP by significantly increasing tail-flick latencies above those of non-EB-treated animals. A similar pattern of increased tail-flick latencies occurred in EB-primed animals that received THDOC. Estradiol benzoate less consistently altered the pain threshold of animals administered P, which is less effective at modulating GABAergic activity. Conversely, EB increased the nociceptive effect of the neurosteroid DHEAS, an allosteric antagonist of GABAA receptor complexes, by significantly decreasing tail-flick latencies of EB-compared to vehicle-primed rats. Thus, EB priming potentiated neuroactive steroids' effects on pain threshold.
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PMID:Estradiol benzoate potentiates neuroactive steroids' effects on pain sensitivity. 884 56

Dermatomes of rats from C1 to T1 (forelimb) and from T12 to S2 (hindlimb) were determined by electrical stimulation of spinal nerves following the intravenous administration of Evans blue. After stimulation of the ventral ramus of a spinal nerve, a blue spotted area presenting the maximal innervation area of the spinal nerve appeared in the skin. Maximal innervation areas generally overlapped the adjacent areas. Each digit was innervated by two to three spinal nerves. Composite dermatomes were determined where boundary lines were defined as the midline of overlapping areas. Based on the composite dermatomes, boundary lines in the rat fore- and hindlimbs were revealed to loop around the antero-posterior axis showing a V-shaped pattern in the anterior and posterior aspects and converge to the ventral and dorsal midlines of the limb. The present dermatome chart may be applied to research concerning the segmental distribution of sensory C-fibers.
Pain 1996 Sep
PMID:Dermatomes in the rat limbs as determined by antidromic stimulation of sensory C-fibers in spinal nerves. 889 48

The present study examined the role of mGluRs in nociceptive responses of male Long-Evans rats following a subcutaneous (s.c.) injection of 1% (30 microliters) or 2.5% (50 microliters) formalin to the plantar surface of the hindpaw. Intrathecal (i.t.) administration of the mGluR4/mGluR6-mGluR8 agonist, L(+)-2-amino-4-phosphonobutyric acid (L-AP4), the mGluR1/mGluR5 antagonists. (S)-4-carboxyphenylglycine ((S)-4CPG) or (S)-4-carboxy-3-hydroxyphenylglycine ((S)-4C3HPG), but not the non-selective antagonist, (+)-alpha-methyl-4-carboxyphenylglycine ((+)-MCPG), to the lumbar spinal cord slightly reduced second phase nociceptive responses. An i.t. injection of the mGluR1/mGluR5 agonist, (RS)-3,5-dihydroxyphenylglycine ((RS)-DHPG) or the mGluR2/mGluR3 agonist, (1S,3S)-1-aminocyclopentane-1,3-dicarboxylic acid ((1S,3S)-ACPD), but not (2S,1'R,2'R,3'R)-2-(2'3-dicarboxy-cyclopropyl)-glycine (DCG-IV), dose-dependently enhanced formalin-induced nociception in the second phase. In addition, the facilitation of nociceptive responses induced by (1S,3S)-ACPD or (RS)-DHPG was reduced by prior i.t. administration of the mGluR antagonists, (+)-MCPG or (S)-4C3HPG, respectively, as well as by the N-Methyl-D-aspartate (NMDA) receptor antagonist, D(-)-2-amino-5-phosphonopentanoic acid (D-AP5). These results indicate that although mGluRs may play a minor role in formalin-induced nociception, mGluR agonist-related facilitation of formalin scores may reflect an interaction with the NMDA receptor.
Pain 1996 Dec
PMID:The contribution of metabotropic glutamate receptors (mGluRs) to formalin-induced nociception. 912 12


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