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

The action of adrenoblocking agents on the dynamics of the pain allaying effect of narcotic analgesics, measured by the magnitude of the pain reaction threshold after irritation of the tail skin with electric current was studies in tests on mice. The beta-adreno-blocking agent (anaprillin or inderal) was found to significantly potentiate and to lengthen the action of morphine, and so did, to a lesser degree, promedol (trimeperedin) and phentanyl, while the alpha-adrenoblocking agent (phentolamine) weakened the analgesic effects of morphine and promedol, without having any essential influence on the effect of phentanyl. Phentolamine does not eliminate the potentiating effect of anapraline on the analgesic action of morphine but is capable to lessen it.
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PMID:[Influence of adrenergic-blocking agents on the pain-alleviating effect of narcotic analgesics]. 2 77

In some patients, ongoing and evoked neurogenic pain is relieved by pharmacological or destructive block of the sympathetic innervation of the affected part. In others, sympatholysis is ineffective. The present report shows that these two groups of patients can be distinguished by a safe and simple diagnostic test. Individuals in whom the pain was transiently relieved by intravenous phentolamine (Regitine) were very likely to respond favourably to subsequent sympatholytic treatment with i.v. regional guanethidine. Individuals in whom the phentolamine test was negative did not enjoy pain relief from this type of sympatholysis.
Pain 1991 Jul
PMID:Intravenous phentolamine test: diagnostic and prognostic use in reflex sympathetic dystrophy. 189 5

Participation of opiate, serotonergic and noradrenergic components in the antinociceptive action of intrathecally administered morphine was evaluated by measuring the ability of subcutaneously administered doses of naloxone, methysergide and phentolamine to alter analgesia. Morphine produced a dose-dependent elevation of the tail-flick latency, due exclusively to local spinal actions. For example, 10 nmol of the drug, when administered intrathecally in rats with bilateral lesions of the dorsolateral funiculus, produced an increase in the tail-flick latency, that was similar to that observed in intact animals. Furthermore, morphine was ineffective when administered intracerebroventricularly into the fourth ventricle of intact rats. The spinal antinociceptive action of the opiate was antagonized by naloxone (ID50 = 0.035 mg/kg, s.c.) but was also significantly attenuated by methysergide (ID50 = 4.28 mg/kg, s.c.). Phentolamine was ineffective. Doses of methysergide that were most effective in reversing the spinal action of morphine also produced hyperalgesia when administered alone. On the other hand, when the dorsolateral funiculus was lesioned, the hyperalgesia was no longer observed, yet the antagonist remained effective against morphine. These data suggested that the doses of methysergide needed to antagonize the action of morphine were in the same range as those needed to block the synaptic actions of serotonin (5-HT) released from the tonically-acting, descending pain inhibitory nerves. The results demonstrate that local opiate, as well as serotonergic, mechanisms mediate the antinociceptive action of morphine in the spinal cord. The recruitment of a serotonergic component may be related to an action of opiates within the spinal cord, to cause the release of serotonin from the terminal fields of the spinipetal serotonergic nerves.
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PMID:A local serotonergic component involved in the spinal antinociceptive action of morphine. 255 80

With electric stimulation of the splanchnic nerve or the skin of the tip of rabbit's ear to measure visceral or somatic pain threshold, we studied the effects of noradrenaline microinjection into the septal nucleus on visceral pain and somatic pain and the relationship between the intraseptal noradrenaline and the intra-PAG opiate peptidergic system. There was no effect on visceral pain threshold after injections of alpha-agonist clonidine (10 micrograms/2 microliters) or alpha-antagonist phentolamine (10 micrograms/2 microliters). In a group injected with beta-agonist isoprenaline (1 micrograms/2 microliters), visceral pain threshold was raised remarkably, while beta-antagonist propranolol (10 micrograms/2 microliters) injected into bilateral septal nuclei decreased visceral pain threshold. Phentolamine (10 micrograms/2 microliters) or propranolol (10 micrograms/2 microliters) injected into septal nucleus induced an elevation of somatic pain threshold. The results indicate that the beta-receptor in spetal nucleus plays an important role in the modulation of visceral pain. Both alpha-and beta- adrenergic receptors have effects on the modulation of somatic pain. Intra-PAG microinjection of naloxone (1 micrograms/1 microliters) attenuated visceral analgesia produced by injection of isoprenaline (1 micrograms/2 microliters) into septal nucleus. Microinjection of anti-leu-enkephalin antiserum (1:20,000) into PAG also attenuated the analgesia. When microinjection of isoprenaline into septal nucleus produced analgesia, the release of leu-enkephalin immunoreactive-like-substance in PAG was significantly increased. The results suggest that the analgesic effect of intra-septal noradrenaline on visceral pain is somehow related with the endogenous opiate peptidergic system in PAG, and the leu-enkephalin in PAG plays an important role in this process.
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PMID:[Effect of intraseptal noradrenaline on somatic and visceral pain threshold of rabbits]. 276 39

Spinal intrathecal injections of the nonsteroidal antiinflammatory analgesics (NSAIAs) indomethacin and acetylsalicylic acid, which inhibit prostaglandin synthesis, cause dose-dependent hypoalgesia in the rat. Intrathecal injections of prostaglandin-E2 (PGE2) produce dose-dependent hyperalgesia. To determine whether this action of prostaglandins on the central nervous system is mediated through pain-generating or analgesia pathways, we studied the effect of intrathecal PGE2 on endogenous opioid-induced analgesia. Intrathecal PGE2 antagonized the analgesia produced by both brain stimulation and intracerebroventricular morphine. In contrast, the NSAIAs synergized with brain stimulation and morphine-induced analgesia. The alpha-adrenergic antagonist phentolamine and the catecholaminergic selective neurotoxin 6-hydroxydopamine, used to block tonic catecholamine activity in endogenous opioid-mediated analgesia systems, prevented the hyperalgesia induced by intrathecal PGE2. Phentolamine did not, however, block the hyperalgesia caused by intradermal PGE2. These findings suggest that prostaglandins can block endogenous opioid-mediated analgesia systems by inhibiting the bulbospinal noradrenergic component of this analgesia pathway.
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PMID:Prostaglandins inhibit endogenous pain control mechanisms by blocking transmission at spinal noradrenergic synapses. 283 84

The effects of the alpha-adrenoceptor antagonists prazosin, phentolamine and yohimbine upon 5-methoxy-N,N-dimethyltryptamine (5-MeODMT)-induced analgesia were tested in the hot-plate, tail-flick and shock-titration tests of nociception with rats. Intrathecally injected yohimbine and phentolamine blocked or attenuated the analgesia produced by systemic administration of 5-MeODMT in all three nociceptive tests. Intrathecally administered prazosin attenuated the analgesic effects of 5-MeODMT in the hot-plate and tail-flick tests, but not in the shock titration test. Intrathecal yohimbine showed a dose-related lowering of pain thresholds in saline and 5-MeODMT-treated animals. Phentolamine and prazosin produced normal dose-related curves in the hot-plate test and biphasic effects in the shock titration and tail-flick tests. These results demonstrate a functional interaction between alpha 2-adrenoceptors and 5-HT agonist-induced analgesia at a spinal level in rats.
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PMID:5-Methoxy-N,N-dimethyltryptamine-induced analgesia is blocked by alpha-adrenoceptor antagonists in rats. 287 97

Focal electrical stimulation in the midbrain periaqueductal gray (PAG) or medullary nucleus raphe magnus (NRM) inhibits spinal nociceptive transmission and nociceptive reflexes. The purpose of this study was to evaluate, in lightly pentobarbital-anesthetized rats, the spinal neurotransmitter(s) mediating descending inhibition of the nociceptive tail-flick (TF) reflex produced by focal electrical stimulation in the PAG or NRM. To characterize the neurotransmitter(s) mediating inhibition of the TF reflex, selective pharmacologic antagonists were administered into the lumbar intrathecal space. Stimulation thresholds in the PAG or NRM for inhibition of the TF reflex were established and the effects of intrathecally administered phentolamine, yohimbine, prazosin, methysergide (15 micrograms initially, 30 micrograms cumulative) or naloxone (10 micrograms initially, 20 micrograms cumulative) on TF inhibitory thresholds determined. Phentolamine, yohimbine and methysergide increased the intensity of stimulation in the PAG and the NRM for inhibition of the TF reflex; prazosin and naloxone had no effect. Descending inhibition produced by focal electrical stimulation in the PAG or NRM is mediated in part by spinal serotonergic and/or alpha 2-adrenergic receptors. Naloxone was administered both intrathecally and intravenously; however, a role for opioid receptors in descending inhibition from the midbrain or medulla was not found.
Pain 1987 Oct
PMID:Stimulation-produced descending inhibition from the periaqueductal gray and nucleus raphe magnus in the rat: mediation by spinal monoamines but not opioids. 289 63

The relative importance of different effector mechanisms of thermoregulation may change depending on their availability. Intact rats make only limited use of a learned response on a cold ambient temperature stimulus, and rely almost entirely on autonomic regulatory functions. After destruction of the anterior hypothalamus, rats exhibit a reduced thermoregulatory capacity; i.e. body temperature drops in the cold and rises in the heat. Under this situation a conditioned operant behavior (lever pressing for increasing or decreasing ambient temperature) becomes an important factor to keep body temperature almost constant. Receptor blockers of some putative transmitters in central thermoregulatory pathways influence thermoregulation. Phentolamine induces hypothermia in intact rats in the cold. Hypothalamic lesions are additive in effect with with the drug. Pimozide has no effect neither in the cold nor in the heat intact and lesioned rats. Biperiden in the heat reinforces hyperthermia in intact and lesioned rats as well; in the cold the drug is ineffective. Performance of lesioned rats in an operant pain titration procedure does not differ from intact rats.
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PMID:Operant thermoregulation of rats with anterior hypothalamic lesions. 732 50

The present study examined antinociception produced by systemic administration of caffeine in the rat hot-plate (HP) and formalin tests and addressed several aspects of the mechanism of action of caffeine. Locomotor activity was monitored throughout. Caffeine produced a dose-related antinociception the HP (50-100 mg/kg) and formalin tests (12.5-75 mg/kg). When observed during the formalin test, caffeine stimulated locomotor activity between 12.5 and 50 mg/kg; this was followed by a depression in activity at 75 mg/kg. Caffeine did not produce an anti-inflammatory effect as determined by hindpaw plethysmometry, suggesting that antinociception was not secondary to an anti-inflammatory action. Peripheral co-administration of caffeine with the formalin did not produce antinociception, suggesting a predominant central rather than peripheral site of action for caffeine. Naloxone (10 mg/kg) did not reduce the antinociceptive or locomotor stimulant effects of caffeine, suggesting a lack of involvement of endogenous opioids in these actions. Phentolamine (5 mg/kg) enhanced antinociception by caffeine in both the HP and formalin tests, but inhibited locomotor stimulation. Prazosin (0.15 mg/kg) mimicked the action of phentolamine on locomotor stimulation, but idazoxan (0.5 mg/kg) mimicked the action of phentolamine on antinociception in the formalin test. These observations suggest an involvement of different alpha-adrenergic receptors in the two actions of phentolamine. Microinjection of 6-hydroxydopamine (6-OHDA) into the locus coeruleus, which depleted noradrenaline (NA) in the spinal cord and forebrain, inhibited the action of caffeine in the HP test. This was mimicked by intrathecal 6-OHDA which depleted NA in the spinal cord, but not by microinjection of 6-OHDA into the dorsal bundle which depleted NA in the forebrain. These results suggest an integral involvement of noradrenergic mechanisms in the antinociceptive action of caffeine in the HP and formalin tests and in locomotor stimulation, but the nature of this involvement differs for the 3 end points.
Pain 1995 May
PMID:Caffeine antinociception in the rat hot-plate and formalin tests and locomotor stimulation: involvement of noradrenergic mechanisms. 765 30

The purpose of this study is to investigate the mechanisms of the effect of hyperventilation on the spinal pain modulating system by using phentolamine. Under enflurane anaesthesia, cats received mid-collicular decerebration and lumbar laminectomy. The spinal cord was transected at T12-L1. WDR cells, responding primarily to noxious peripheral stimuli, were sampled with a microelectrode at the depth of 2,000 microns from the cord dorsum. Following the control period, ventilation was changed to induce hypocapnia of PCO2 20-25 mmHg. After activities were well suppressed, phentolamine 0.5 mg with normal saline 1.0 ml was injected on the spinal cord. Changes of firings were investigated. When normocapnia was resumed, recovery followed. Hypocapnia of PCO2 20-25 mmHg significantly suppressed the activities of WDR cells. Phentolamine significantly antagonized the suppressive effects of hyperventilation upon the activities of WDR cells. Our results suggest that the hyperventilation has suppressive effects on single-unit activity of WDR cell and the mechanisms of those suppressive effects are related to adrenergic pain modulating system.
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PMID:[Effects of hyperventilation upon the spinal pain modulating system (third report)]. 781 94


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