Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of alpha 1 receptors in antinociception was investigated in the formalin test, a well established test of tonic pain. The effect of systemic injections of selective alpha 1-adrenergic agonists (phenylephrine and methoxamine), a mixed alpha agonist selective for alpha 2 receptors (ST-91), and 2 adrenergic antagonists (prazosin and idazoxan) was measured in groups of Long-Evans rats. All agonists tested produced significant antinociception in this test. Dose-response curves for each agonist were statistically parallel and equally efficacious (100% antinociception). Prior injection of 0.15 mg/kg prazosin (an alpha 1 antagonist) completely antagonized the antinociception produced by either an ED50 or a maximally effective dose of each agonist tested. Idazoxan (0.5 mg/kg), an alpha 2 antagonist, was without effect on the antinociception produced by phenylephrine or methoxamine. ST-91 produced significant antinociception in the presence of idazoxan although the response was different from that obtained with ST-91 alone. The observed antinociception in the formalin test was not due to drug-induced changes in peripheral inflammation as measured using plethysmometry. Moreover, none of the drugs tested produced significant changes in coordinated motor behavior (accelerated rotarod test) at doses that produced significant analgesia (ED50). We conclude that alpha 1 receptors contribute significantly to adrenergic analgesia in the formalin test by an undefined action on sensory processing mechanisms.
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PMID:Systemic injections of alpha-1 adrenergic agonists produce antinociception in the formalin test. 135 19

Ingestion of placenta and amniotic fluid has been shown to enhance opioid-mediated analgesia in rats produced by morphine injection, footshock, vaginal/cervical stimulation, and during late pregnancy. The present study was designed to investigate the effects of amniotic fluid ingestion on the characteristics of morphine dependency and withdrawal. Tail-flick latencies in Long-Evans rats were determined before and after repeated daily injections of morphine sulfate. It was found that ingestion of amniotic fluid after establishment of the morphine dependency, coupled with an injection of an otherwise ineffective dose of morphine, enhanced analgesia in morphine-dependent rats, and reversed hyperalgesia seen during withdrawal from morphine dependency.
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PMID:Amniotic-fluid ingestion enhances morphine analgesia during morphine tolerance and withdrawal in rats. 180 Oct 21

The analgesic effect of electrical stimulation of the hypothalamic paraventricular nucleus (PVN) was studied. Additionally, the involvement of vasopressin and opioid peptides in this process was examined by comparing vasopressin-deficient (Brattleboro) and Long-Evans rats and by administering the opiate antagonist naloxone. Rats were chronically implanted with a stimulating electrode in the parvocellular (PVN-Pc) and magnocellular (PVN-Mg) divisions of the PVN. At least 10 days after surgery, the analgesic effects of PVN stimulation were examined in lightly anesthetized rats, using the tail-flick method, and in unanesthetized rats, using the hot-plate test. PVN stimulation produced marked analgesia in both tests. Current threshold for analgesia was lower from PVN-Pc than from PVN-Mg. Threshold did not differ significantly between Brattleboro and Long-Evans rats and was not affected by naloxone administration. The results indicate that the PVN is part of the brain's pain inhibitory system, and show that the analgesia induced by PVN stimulation is not mediated by either vasopressin or opioid peptides.
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PMID:Stimulation of the hypothalamic paraventricular nucleus produces analgesia not mediated by vasopressin or endogenous opioids. 198 39

AHR-10037 is an anti-inflammatory compound possessing analgesic and antipyretic properties and a high therapeutic index. AHR-10037 was comparable to indomethacin in suppressing acute (Evans blue-carrageenan pleural effusion) and chronic (adjuvant-induced arthritis) inflammation. There was a delayed onset of antipyresis (yeast-induced hyperthermia in rats), analgesia (acetylcholine-induced abdominal constriction in mice) and inhibition of caster oil-induced diarrhea in rats. Antipyresis occurred 3 hours after administration of AHR-10037, 4 mg/kg, PO. vs 1 hour after administration of acetylsalicylic acid, 100 mg/kg, PO; maximum analgesic activity (ED50 = 4.1 mg/kg) occurred at 4 hours. AHR-10037 was inferior to indomethacin in suppressing castor oil-induced diarrhea in rats. The therapeutic index of AHR-10037 (relating acute anti-inflammatory potency to gastric toxicity potency relative to indomethacin) ranged from 56-91. The pharmacological profile suggests that AHR-10037 is a prodrug converted in vivo to a cyclooxygenase inhibitor.
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PMID:AHR-10037, a non-steroidal anti-inflammatory compound of low gastric toxicity. 228 17

In the present experiments the role of unmyelinated sensory fibres in the mechanism of cutaneous inflammatory reactions under normal and pathological conditions has been studied in man and animals. Dye leakage responses to histamine, serotonin, compound 48/80, bradykinin and substance P were significantly reduced, while neurogenic inflammation was completely abolished in rats treated neonatally with capsaicin, as studied quantitatively by the Evans blue technique. Neurogenic inflammation could also be elicited by mustard oil in normally innervated human skin, but not in skin areas affected by herpes zoster or in a patient suffering from congenital analgesia. Repeated topical treatment of the skin with capsaicin (local desensitization) abolished the neurogenic inflammatory response for several days. Chemical pain sensitivity was strongly reduced, and thresholds for warmth and heat pain sensations were significantly elevated. Local capsaicin desensitization of the skin prevented whealing, flare and itch in patients with acquired cold and heat urticaria. The findings indicate that peptide-containing sensory nerves are involved in the mediation of chemogenic and heat pain, and possibly itch, and are responsible for initiation of the neurogenic inflammatory response. The results also provide direct evidence of the involvement of these particular sensory nerves in the modulation of the permeability-increasing effects of putative mediators of acute inflammatory reactions. It is concluded that, through modulation of cutaneous vascular reactions, peptidergic sensory nerves may play a hitherto unrecognized role in the pathomechanism of certain diseases of human skin.
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PMID:The modulation of cutaneous inflammatory reactions by peptide-containing sensory nerves. 241 73

Ingestion of placenta and amniotic fluid has been shown to enhance opioid-mediated analgesia produced by morphine injection, footshock, vaginal/cervical stimulation, and during late pregnancy in rats. The present study was designed to determine how soon after ingestion the enhancement begins and how long it lasts. Tail-flick latencies in Long-Evans rats were determined before and during vaginal/cervical stimulation; analgesia was measured as the percent increase in tail-flick latency during vaginal stimulation. After determination of baseline, rats were intubated with 0.25 ml of either amniotic fluid or beef bouillon. We found that analgesia enhancement was detectable as early as 5 minutes after ingestion of amniotic fluid, and the effect lasted at least 30 minutes, but no longer than 40 minutes.
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PMID:Enhancement of opioid-mediated analgesia by ingestion of amniotic fluid: onset latency and duration. 251 10

The ability of both naloxone and naltrexone to block conditional analgesia produced by shock associated contextual stimuli was determined using rats from three suppliers. Naltrexone (7 mg/kg) was equally effective in reversing analgesia on the formalin test in all rats tested. Naloxone (7 mg/kg) significantly affected analgesia in Long-Evans and Holtzman Sprague-Dawley rats but had no effect on Charles River (CD) Sprague-Dawley rats. Charles River rats also differed from the other groups in the amount of time spent freezing to apparatus cues. These results indicate that genetic factors and the choice of antagonists may complicate distinctions between opioid and nonopioid analgesia.
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PMID:Strain differences in reversal of conditional analgesia by opioid antagonists. 367 53

Placenta ingestion has recently been shown to enhance opiate-mediated analgesia produced by morphine injection, footshock, or vaginal/cervical stimulation. The enhancement of the effect of endogenous opiates (especially analgesia) may be one of the principal benefits to mammalian mothers of placentophagia at delivery. During labor and delivery, however, mothers also ingest amniotic fluid (AF) which, unlike placenta, becomes available during, or even before expulsion of the infant. The present experiments were undertaken to determine whether AF ingestion, too, enhances analgesia; if so, whether the effect requires ingestion of, or merely exposure to, AF; whether the effect can be produced by AF delivered directly to the stomach by tube; and whether the enhancement, if it exists, can be blocked by administering an opiate antagonist. Nulliparous Long-Evans rats were tested for analgesia using tail-flick latency. We found that rats that ingested AF after receiving a morphine injection showed significantly more analgesia than did rats that ingested a control substance; AF ingestion, alone, did not produce analgesia; ingestion of AF, rather than just smelling and seeing it, was necessary to produce analgesia enhancement; AF produced enhancement when oropharyngeal factors were eliminated by delivering it through an orogastric tube; and treatment of the rats with naltrexone blocked the enhancement of morphine-induced analgesia that results from AF ingestion.
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PMID:Ingestion of amniotic fluid enhances opiate analgesia in rats. 382 99

Experiments were carried out to investigate whether vasopressin is involved in stress-induced analgesia. Intraperitoneal injection of hypertonic saline caused a significant and dose-related increase in the latency to the tail-flick response of the rat to noxious heat and was used as a stimulus for stress-induced analgesia. Neither the pituitary nor opioid peptides appeared to be involved, since the response occurred in hypophysectomized rats and was not reduced by the opiate antagonist naloxone. Furthermore hypertonic-saline analgesia was clearly potentiated in hypophysectomized rats in comparison to sham-operated controls. Hypertonic-saline analgesia was also observed in vasopressin-deficient (homozygous Brattleboro) rats similar in both magnitude and duration to that in normal rats of the same strain (Long Evans). It was concluded that vasopressin was not involved in stress-induced analgesia evoked by hypertonic saline.
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PMID:Stress-induced analgesia evoked by intraperitoneal injection of hypertonic saline: evidence for its occurrence in vasopressin deficient rats. 403 7

Retrograde transport of the fluorescent dyes Evans blue and 4,6-diamidino-2-phenyl indole (DAPI) has been used to study projections from the medullary raphe nuclei to the trigeminal nucleus caudalis and to the dorsolateral quadrant of the thoracolumbar cord in the rat. The majority of projecting neurones were found in n. raphe magnus (NRM) and its ventrolateral extensions over the pyramids and inferior olive. Double labelling experiments showed that 94% of raphe-trigeminal neurones sent a collateral branch to the nucleus in the contralateral brainstem. Similarly, 92% of raphe-trigeminal neurones branched to supply the thoracolumbar cord. It is suggested that the widespread nature of the analgesia produced by electrical stimulation in NRM in conscious animals may be due to activation of a population of raphe neurones which inhibit the responses of neurones in the trigeminal nucleus and dorsal horn via an extensive system of collateral projections to these structures.
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PMID:Bulbar raphe neurones with projections to the trigeminal nucleus caudalis and the lumbar cord in the rat: a fluorescence double-labelling study. 664 62


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