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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exposing mice to 24 and 4 degrees C in alternate 1 hr periods in the day time and maintaining 4 degrees C at night for several days decreases the tail clamp pressure required to evoke pain behavior. This model is referred to as SART (specific alternation rhythm of temperature) stress. An extract from inflamed skin of rabbits inoculated with vaccinia virus (neurotropin) clearly normalized the hyperalgesia in this SART stress model. To clarify the mechanism of the hyperalgesia in SART mice and the mode of the antinociceptive action of neurotropin in this model, the influence of systemically administered neurotransmitter related drugs was studied. 1) Neurotropin, 5-hydroxytryptophan and L-dihydroxyphenylalanine significantly normalized the decrease in nociceptive threshold, and muscimol tended to inhibit it in nociceptive threshold in SART stressed mice. 2) Haloperidol, phenoxybenzamine, reserpine, bicuculline, scopolamine, physostigmine and naloxone alone did not influence the nociceptive threshold in SART stressed mice. 3) The antinociceptive effect of neurotropin was significantly attenuated by p-chlorophenylalanine, haloperidol and phenoxybenzamine; and it was completely inhibited by reserpine. 4) Naloxone, bicuculline, scopolamine and physostigmine had no influence on the antinociceptive effect of neurotropin. These results suggest that hypofunction mainly of the monoaminergic systems contributes to hyperalgesia in SART stressed mice and that neurotropin produces the antinociceptive effect by restoring these neural functions.
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PMID:Mechanism of hyperalgesia in SART stressed (repeated cold stress) mice: antinociceptive effect of neurotropin. 183 38

A majority of patients experience pruritus, nausea and/or emesis following epidural morphine administration post-cesarean section. Naloxone or diphenhydramine are commonly used to treat these side effects. Prevention or reduction in the incidence of side effects of epidural morphine is a clinical goal. The purpose of the study was to observe the efficacy of prophylactic administration of hydroxyzine on the incidence and severity of pruritus following the epidural administration of morphine in 40 patients who requested epidural morphine for postoperative pain relief. Group I (n = 20) received saline, while Group II (n = 20) received 50 mg of hydroxyzine ten minutes after the administration of 5 mg epidural morphine. Both solutions were administered by deep intramuscular injection in the thigh area. The results of this investigation demonstrated that hydroxyzine was efficacious in attenuating the incidence of severe pruritus.
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PMID:Epidural morphine pruritus reduction with hydroxyzine in parturients. 191 5

A controversy exists concerning the role of the neuropeptide somatostatin for the transmission or inhibition of nociceptive information in the spinal cord. To better correlate electrophysiological effects of somatostatin at single cell level with results obtained with intrathecal injections of somatostatin in behaving animals and human pain patients we applied somatostatin to the spinal cord by controlled superfusion of the recording segment in vivo. The hypothesis of an opioid link and possible neurotoxic effects of somatostatin were also addressed. In cats deeply anaesthetized with pentobarbitone, halothane and nitrous oxide, extracellular recordings were made from 27 neurons located in laminae I-VI. All neurons responded to both innocuous mechanical and noxious radiant heat stimuli applied to the glabrous skin of the ipsilateral hindpaw. The dorsal surface of the spinal cord was superfused at the recording segment by means of a Perspex chamber (7 x 7 mm). Somatostatin superfusions at 1.2 microM had no effect on responses to noxious heat. Responses were, however, depressed by somatostatin at 61 microM to 59.7 +/- 5.1% of control and by somatostatin at 1.53 mM to 39.9 +/- 9.5% of control. This inhibition was not antagonized by the mu-opiate antagonist naloxone applied to the spinal cord at concentrations of 2.7 mM, either together with somatostatin, or after the inhibition by somatostatin had fully developed. Neuronal responses were linear functions of the skin temperatures for stimulation intensities between 42 degrees C and 52 degrees C. The slopes of these stimulus response functions were reduced during somatostatin superfusion at 61 microM to 46.8 +/- 9.3% of control, without changing the temperature thresholds for responding (42.5 +/- 0.6 degrees C). Somatostatin superfusion at 61 microM had no effect on the number of action potentials evoked by innocuous skin brushing, or by electrical stimulation of primary afferent A-fibres in cutaneous nerves. The amplitude of intraspinally recorded field potentials evoked by these electrical nerve stimuli was also unaffected by somatostatin. The inhibition of nociceptive spinal dorsal horn neurons by spinally administered morphine was assessed in eight experiments. Morphine reduced noxious heat-evoked responses to 42.1 +/- 9.6% of control at 0.3 mM and to 51.8 +/- 6.9% of control at 3.0 mM. The slopes of the stimulus-response functions were reduced by morphine at 0.3 mM to 53.1 +/- 11.3% of control, without changing the temperature thresholds (42.7 degrees C). Naloxone superfusion (2.7 mM) reliably antagonized the inhibition by morphine. Brush-evoked responses were not, or much less, affected by spinal morphine.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Spinal somatostatin superfusion in vivo affects activity of cat nociceptive dorsal horn neurons: comparison with spinal morphine. 197 67

The ionizing radiation (150 Gy) extended the rat tail flick latency, decreased the pain-relief effects of morphine and opioids and enhanced the analgesic effect of clopheline. The radiation was followed by a decrease of vocalization threshold with a reduction of morphine- and clopheline-induced analgesia. Naloxone (0.1 mg/kg) eliminated the postradiation analgesia and did not change the hyperalgesic effect of the radiation.
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PMID:[The analgesic action of narcotic analgesics and clopheline after the ionizing irradiation of rats]. 198 87

Experimental pain thresholds (electrical intracutaneous finger and dental pulp stimulation) and plasma hormone levels (beta-endorphin, cortisol, and catecholamines) were measured in ten healthy sportive men before, during, and after progressively more strenuous physical exercise. In a double-blind study conducted on two different days, 20 mg of the opioid-antagonist naloxone or placebo was administered prior to exercise. A significant pain threshold elevation was found during exercise for finger (ANOVA, P less than 0.004) and dental pulp stimulation (P less than 0.01). Pain threshold elevation was most pronounced during maximal exertion, at which time the subjects reported the greatest subjective fatigue. Thresholds remained elevated 10-15 min after the end of exercise, and, 60 min after exercise, thresholds returned to baseline values. The subjective magnitude estimation of suprathreshold stimuli was significantly reduced (P less than 0.0001) 5-10 min after exercise. Plasma beta-endorphin, cortisol, and catecholamines increased significantly (P less than 0.0005, all values) during exercise. Plasma beta-endorphin levels did not correlate significantly with pain thresholds (r = -0.37, NS). Naloxone failed to affect pain thresholds, although beta-endorphin and cortisol increased significantly more (P less than 0.02) during exercise after naloxone. It is concluded that short-term, exhaustive physical exercise can evoke a transient elevation in pain thresholds. This exercise-induced elevation in pain threshold does not, however, appear to be directly related to plasma endorphin levels.
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PMID:Experimental pain thresholds and plasma beta-endorphin levels during exercise. 202 Feb 72

The studies were done to determine whether inhibition of the tail-flick response induced by beta-endorphin and morphine microinjected into periaqueductal central gray (CG) was mediated by stimulating different types of opioid receptors and by activating different descending pain modulatory systems in rats. beta-Endorphin (0.3-20 micrograms) or morphine (0.3-20 micrograms) microinjected bilaterally into CG produced a dose-dependent inhibition of the tail-flick response. Naloxone (0.3-3 micrograms) injected into CG was more effective in antagonizing inhibition of the tail-flick response induced by CG administered morphine than by beta-endorphin. beta-Endorphin-(1-27) (3 micrograms) injected CG effectively antagonized CG beta-endorphin-induced inhibition of the tail-flick response but slightly potentiated CG morphine-induced inhibition. Intrathecal injection of naloxone (0.3-30 micrograms) dose-dependently reversed inhibition of the tail-flick response induced by beta-endorphin (2 micrograms) but not by morphine (4 micrograms) injected into CG. On the other hand, yohimbine (0.3-30 micrograms) injected intrathecally dose-dependently antagonized inhibition of the tail-flick response induced by morphine (4 micrograms) but not by beta-endorphin (2 micrograms) given into CG. It was concluded that beta-endorphin and morphine produce inhibitions of the tail-flick response by stimulating epsilon and mu opioid receptors, respectively, and the descending pain modulatory system activated by beta-endorphin from CG involves spinal opioid receptors but not alpha-2 adrenoceptors whereas the descending system activated by morphine from CG involves spinal alpha-2 adrenoceptors but not opioid receptors.
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PMID:Different mechanisms mediate beta-endorphin- and morphine-induced inhibition of the tail-flick response in rats. 215 50

Rats were subcutaneously implanted with minipumps delivering naloxone (3.0 mg/kg/h) or distilled water. One day later, they were inoculated in the plantar surface of the right hind paw with Mycobacterium butyricum. Naloxone blocked the antinociceptive action of the mu-agonist, morphine, and the kappa-agonist, U69,593, and led to a sustained reduction in food and water intake. Thus, opioid receptors were effectively occupied. Rats receiving naloxone showed significantly less hindlimb swelling on days 2 and 3 post-implantation. On day 2 but not 5 post-implantation, the hyperalgesic response of the inoculated paw to noxious pressure was potentiated in rats receiving naloxone. At six days post-implantation, pumps were removed. Ten days after removal, the inflammation and hyperalgesia had spread to the contralateral hindlimb and to the forelimbs. The degree of this transfer was less pronounced in rats which had been receiving naloxone. These data suggest that opioids, via kappa-receptors, play a role in the control of nociception under inflammatory pain: however, this role may not be indispensable. Further, the processes governing the development and spread of inflammatory disease may be modulated by opioid mechanisms.
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PMID:The influence of sustained opioid receptor blockade in a model of long-term, localized inflammatory pain in rats. 216 76

Tethered sows, some of which performed marked behavioral stereotypies after feeding, were injected IM with 1 mg/kg of naloxone 30 min before feeding (with 2 saline control days). Tail-flick latencies on a pain-sensitivity test were recorded before and after feeding. On control days, tail-flick latencies after feeding were longer than those before feeding, and this effect was abolished by naloxone pretreatment. Thus, there is an opioid-based hypoalgesia after feeding. However, sows with marked behavioral stereotypies had shorter tail-flick latencies after feeding. Thus, we have no evidence that performance of behavioral stereotypies results in increased opioid activity. Naloxone reduced the time spent in behavioral stereotypies by approximately 30% but this may be due to a reduction in time spent active. Naloxone increased the frequency and reduced the mean duration of bouts of chain manipulating, operating the drinker and rooting. We suggest that endogenous opioids are involved in the positive feedback that maintains the persistence of behavior and inhibits switching between different activities.
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PMID:Stereotypic behavior, endogenous opioids, and postfeeding hypoalgesia in pigs. 217 7

Study of the effect of naloxone that blocks opiate receptors on changes in thresholds of vocalization and latent periods of motile reaction in freely-behaving rats, at leg injury, intraperitoneal introduction of algogene, and at immobilization stress allowed to estimate the involvement of endogenous opiates in regulation of pain sensitivity and motile activity. Naloxone-weakened inhibition of vocalization is accompanied by the increase in inhibition of motile responses, characteristic for visceral pain and the absence of changes at trauma and immobilization stress suggest that opiates are involved in formation of endogenous analgesia at strong visceral pain stimulation.
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PMID:[Endogenous opioid mechanisms in the regulation of pain sensitivity and behavioral reactivity in various aversive states]. 217 67

Experimental data indicate that clonidine can induce marked analgesia. We characterized this effect in healthy volunteers and investigated possible links with the opioid peptide system by means of naloxone antagonism. According to a cross-over, double-blind, placebo-controlled design, 10 subjects received oral and i.v. placebo or clonidine (0.2 mg p.o.) or clonidine and naloxone (2.8 mg i.v. in 5 h). Analgesia was assessed by measurement of the subjective pain threshold (visual analog scale) and the objective nociceptive flexion reflex (R III) threshold after transcutaneous electrical stimulations. A correlation was observed between subjective and objective thresholds (r: 0.78). Oral clonidine alone or with naloxone increased subjective and objective pain thresholds for at least 4 hours (p less than 0.01, ANOVA). Naloxone tended to reinforce clonidine analgesia. Only moderate and well tolerated side-effects were observed.
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PMID:Objective assessment of clonidine analgesia in man and influence of naloxone. 218 59


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