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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mice selectively bred for high (HA) and low (LA) swim-induced analgesia were exposed to two different stress paradigms; one consisting of a 3-min swim at 20 degrees C daily for 14 days, and the other consisting of 3-min swims repeated at 2-h intervals for 48 h. Both forms of chronic stress resulted in the development of tolerance to swim-induced antinociception to a greater degree in the HA mice than in control (C) mice, but were both ineffective at inducing tolerance in LA mice. Swimming repeated at 2-h intervals for 48 h resulted in cross-tolerance with morphine in HA and C mice. Naloxone (1 and 10 mg/kg, IP) failed to antagonize swim-induced analgesia in mice that had experienced chronic swimming in the 2-h/48-h paradigm. The daily swimming paradigm failed to produce cross-tolerance with morphine analgesia in any line. Differential degree of tolerance in three lines supports a hypothesis that selective breeding for high and low stress-induced analgesia has modified the degree of opioid involvement in the endogenous analgesia mechanisms.
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PMID:Tolerance and cross-tolerance with morphine in mice selectively bred for high and low stress-induced analgesia. 180 31

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

This is one of a series of experiments designed to examine the possible pharmacologic basis for analgesia normally associated with pregnancy. The antinociceptive effects of low-dose (0.1 mg/kg) subcutaneous clonidine on analgesia associated with pregnancy were evaluated in rats. Colorectal distention thresholds and tail-flick latencies were determined in timed pregnant rats (n = 27) before mating, on days 7 and 21 of gestation, and on postpartum day 7. Immediately after baseline testing on each of those days, animals received 0.1 mg/kg clonidine subcutaneously and were retested 30 min later. On day 21 of gestation, 20 micrograms/kg naloxone (n = 9) and 0.2 mg/kg yohimbine (n = 5) were intravenously administered after clonidine testing, and animals were retested 15 min later. In the absence of clonidine, pregnant animals demonstrated a statistically significant increase in their tolerance of colorectal distention pressures and longer latencies to tail-flick withdrawal on day 21 of gestation. Clonidine produced a further significant increase in distention thresholds on day 21 of gestation but did not change these thresholds on any other day, nor did it change tail-flick latencies. Naloxone and yohimbine reversed the effect of clonidine on the distention thresholds on day 21. Systemic clonidine, at a dose lower than that required to produce antinociception in nonpregnant rats, enhanced pregnancy-induced analgesia to visceral stimulation late in pregnancy, an effect that was reversed by naloxone and yohimbine. These results suggest a synergistic antinociceptive effect of clonidine due to an interaction with an endogenous opiate system that is only activated late in pregnancy.
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PMID:Low-dose clonidine enhances pregnancy-induced analgesia to visceral but not somatic stimuli in rats. 199 61

The effects of lappaconitine (LA) and N-deacetyllappaconitine (DLA) on footshock-induced analgesia (FSIA) were studied by the rat tail flick test. Rats subjected to 90 s nonescaping footshock had a significant increase in tail flick latency. Naloxone (4 micrograms, i.c.v.) partially antagonized the FSIA. After 5 consecutive exposures to footshock, rats developed a complete tolerance to the FSIA. The rats tolerant to FSIA showed a cross-tolerance to morphine- but not LA- and DLA-induced analgesia. Administrations of subanalgesic doses of LA and DLA potentiated the FSIA in both intact and adrenalectomized rats.
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PMID:Lappaconitine and N-deacetyllappaconitine potentiate footshock-induced analgesia in rats. 200 53

Noradrenergic neuronal hyperactivity following chronic morphine administration has been postulated to cause withdrawal signs and symptoms. Suppression of this hyperactivity, for example, by clonidine attenuates withdrawal. It might follow, therefore, that the prevention of suppression of noradrenergic systems during chronic morphine administration might diminish hyperactivity and prevent withdrawal. If the normalization of noradrenergic activity during opioid administration did not also suppress analgesia, it might be of medical and theoretical interest. To test this hypothesis, we gave the alpha-2-antagonist yohimbine to rats in order to increase noradrenergic activity during morphine treatment and then subsequently precipitated morphine withdrawal with naloxone. Six groups were examined: saline controls (N = 11), morphine (N = 11), morphine + 2.0 mg/kg/day yohimbine (N = 15), morphine + 3.0 mg/kg/day yohimbine (N = 5), 2.0 mg/kg/day yohimbine (N = 11) and 3.0 mg/kg/day yohimbine (N = 5). Subjects received 75 mg morphine pellets implanted on day 1,4 and 6 of the treatment or sham implantation. Yohimbine was delivered throughout the morphine treatment by subcutaneously implanted osmotic pumps. On day 7, all subjects were given 1.0 mg/kg naloxone and rated for behavioral signs of withdrawal. Analgesia was measured by observing tail flick latencies (TFL) before and after chronic drug treatments. Naloxone-precipitated withdrawal was characterized by irritability, ptosis, penile erection, diarrhea, rhinorrhea, abnormal posture, wet-dog shakes, jumping, and teeth chattering, none of which were observed in groups receiving only saline or yohimbine. Withdrawal behavior was attenuated in a dose-dependent manner when yohimbine was administered during morphine treatment but analgesia was not attenuated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Yohimbine co-treatment during chronic morphine administration attenuates naloxone-precipitated withdrawal without diminishing tail-flick analgesia in rats. 205 41

Two experiments were made showing that opioid involvement coincides with the magnitude of stress-induced analgesia. In Experiment I rats subjected to cold water swims were screened for jump threshold levels on electrified grid and divided into high, medium and low threshold responders' groups. Later on the three groups were given 90 s forepaw footshock. Tail-flick latencies rose highest in the high threshold, and lowest in the low threshold responders. This decrease in nociception was counteracted by naloxone more effectively in high than in medium threshold responders, and not all in low threshold responders. In Experiment II mice selectively bred for high (HA) and low (LA) post-stress analgesia swam at 20 and 2 degrees C. Both stressors were followed by an increase in tail-flick latencies in the order of magnitude HA greater than unselected controls greater than LA line. Naloxone attenuated analgesia after both stressors in the HA line, but was ineffective in LA mice. In unselected controls swimming at 20 degrees C caused naloxone-sensitive, and cold water swims naloxone-resistant analgesia. It is concluded that apart from the kind of stressor, inborn properties of an individual are essential for the development of opioid vs. non-opioid form of post-stress analgesia.
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PMID:Correlation between magnitude and opioid mediation of stress-induced analgesia: individual differences and the effect of selective breeding. 213 37

The analgesic effect of electrical stimulation of the periaqueductal gray matter (PAG) was studied in 4 strains of mice: C57BL/6By (C57), BALB/cBy (BALB), CXBH, and CXBK. These strains are known to have high (CXBH), low (CXBK), and intermediate (C57 and BALB) concentrations of brain opiate receptors. The current intensity required for stimulation-produced analgesia (SPA) did not differ among strains. Naloxone attenuated SPA in CXBH, C57 and BALB mice, but was ineffective in the opiate receptor deficient CXBK mice. The results suggest that genetic differences in opiate receptor density can influence the degree to which opioid mechanisms are involved in SPA from the PAG.
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PMID:Genetic influences on brain stimulation-produced analgesia in mice: II. Correlation with brain opiate receptor concentration. 215 97

Naloxone (Narcan), a semisynthetic opioid antagonist, has approved therapeutic use for the treatment of opioid-induced central nervous system depression. With the implementation of epidural and intrathecal opioid analgesia, naloxone has been used for the treatment of side effects associated with these methods of analgesia. Consequently, there has been greater utility of naloxone for postoperative orthopaedic, noncritical patients. Naloxone was thought to be devoid of any intrinsic activity and, therefore, thought to have few side effects. There have been several reports of cardiovascular complications associated with naloxone administration that have disputed this view. Since use of naloxone is increasing in orthopaedic nursing practice, orthopaedic nurses need to understand the potential complications associated with its use.
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PMID:Naloxone: a word of caution. 216 31

Naloxone benzoylhydrazone (NalBzoH) is a novel mixed agonist/antagonist. Against mu agonists, NalBzoH is a potent antagonist with a prolonged duration of action corresponding to its extremely slow rate of dissociation from mu receptors in binding assays. In the present studies, NalBzoH also antagonized mu analgesia, reversing both mu 1 and mu 2 analgesia independently elicited by intracerebroventricular or intrathecal [D-Ala2,MePhe4,-Gly(ol)5]enkephalin injections. It also antagonized kappa 1 analgesia elicited by U50,488H, and delta analgesia produced by intrathecal [D-Pen2,D-Pen5]enkephalin. Yet, at higher doses, NalBzoH alone produced analgesia in the tail-flick, hot plate and writhing assays. Neither the mu-selective antagonist beta-funaltrexamine, the delta-selective antagonist naltrindole, nor the kappa 1-selective antagonist norbinaltorphimine reversed NalBzoH analgesia in the tail-flick test. Analgesia observed with systemically administered NalBzoH was reversed easily by the antagonist WIN44,441 when it was given intracerebroventricularly, but not intrathecally. These observations confirm the opioid nature of NalBzoH analgesia and imply a supraspinal mechanism of action. In contrast, intrathecal, but not intracerebroventricular WIN44,441 reversed analgesia from systemic U50,488H quite potently. Thus, NalBzoH antagonizes mu, delta and kappa 1 actions while retaining its ability to elicit analgesia through a novel and distinct supraspinal kappa 3 system.
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PMID:Naloxone benzoylhydrazone (NalBzoH) analgesia. 217 57

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


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