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)

Effects of drugs that modify catecholaminergic or tryptaminergic mechanisms were determined in experimental animals regarding the analgesic action of difenamizole, morphine, and aminopyrine. Analgesia was assessed by the hot plate method in mice and the hot water induced tail withdrawal reflex in rats. Both 5-hydroxytryptophan (5-HTP) and L-dopa potentiated the analgesic action of morphine, but antagonized the action of difenamizole in the hot plate test. p-Chlorophenylalanine (pCPA), alpha-methyl-p-tyrosine (alpha-MT), and reserpine antagonized the effect of morphine as assessed by this same test. alpha-MT potentiated the analgesic action of difenamizole. The analgesic action of aminopyrine was hardly modified in the hot plate method by pretreatment with 5-HTP, pCPA, L-dopa, and alpha-MT. In rats, 5-HTP antagonized the effect of morphine, while pCPA, L-dopa, and alpha-MT caused no appreciable change in the analgesic action of morphine in the hot water induced tail withdrawal reflex. The effect of difenamizole was not modified by pretreatment with these monoamine-related drugs. On the other hand, brain 5-hydroxytryptamine content was increased by pretreatment with 5-HTP in both tests. These results suggest that the analgesic action of difenamizole and morphine, as measured in the hot plate test in mice, may be mediated by catecholamines and 5-hydroxytryptamine, but that other mechanisms may be involved in the hot water induced tail withdrawal relfex in rats. In addition, the biogenic amines may play a different role depending on the type of analgesic.
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PMID:[Relationship between biogenic amines and analgesic action of difenamizole in heat induced reflexes]. 13 90

In a previous work (4), it has been described that a noxious visceral stimulation through the intraperitoneal injection of acetic acid (ipAA) induced a transient and low magnitude increase in tail-flick latencies, but a marked increase in the threshold for vocalization and hot-plate latencies. In the present work, this phenomenon of hypoalgesia through counter-irritation was investigated in intact rats with or without pretreatment with the potent serotonin depletor parachlorophenylalanine (pCPA). Three behavioural tests were performed. In two tests (tail flick, vocalization induced by transcutaneous electrical stimulation of the tail), pCPA pretreatment induced an increase of baseline levels, before IP injection of the allogenic agent (ipAA). In the third test, pCPA pretreatment had no effects on jump latencies. Parachlorophenylalanine pretreatment had no effect upon hypoalgesic actions of IP injected AA in all three tests. These results are discussed in terms of pCPA's differential effects upon basal nociception and analgesia induced by various heterotopic nociceptive stimulations.
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PMID:Hypoalgesia induced by counter-irritation is not affected by pCPA pretreatment. 214 Jan 96

To explore the neuroanatomical pathways involved in mediating the antipropulsive effect and analgesia of morphine (M) in the periaqueductal gray matter (PAG), we examined the influence of the vagus nerve and the role of serotonergic neurotransmission. M-induced inhibition of intestinal transit was unaffected by subdiaphragmatic vagotomy. In contrast, electrolytic lesions in the raphe magnus nucleus (NRM) and pretreatment with a selective neurotoxin (5,6-DHT, 15 micrograms/rat) in the same region, both significantly reduced M-induced inhibition of intestinal transit. Analgesia was only slightly affected. p-CPA pretreatment (100 mg/kg IP) induced the same results. Finally some other central brain regions were found to be sensitive to M's intestinal inhibition and analgesia such as the mid-line thalamus, the dorsal and lateral hypothalamus, and the bulbar reticular formation. Negative results were obtained for frontal cortex, caudate and amygdala. Some considerations are put forward about the existence in the central nervous system of selective areas involved in intestinal modulation and their relation with those mediating pain transmission.
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PMID:Supraspinal cerebral areas involved in morphine's intestinal inhibition and analgesia. 317 62

p-Chlorophenylalanine (p-CPA) reduces brain 5-hydroxytryptamine (5-HT) without altering the dopamine and norepinephrine content. Morphine does not influence the 5-HT level, but partly reverses the depletion of 5-HT by p-CPA. Morphine analgesia and toxicity are not affected by p-CPA treatment. p-CPA also has no effect on acute morphine hypothermia, but after chronic treatment of 5-HT-deficient mice the dose--response curve is no longer parallel, which suggests that another mode of morphine hypothermia occurs. p-CPA diminishes morphine-induced running after acute as well as after chronic morphine administration. p-CPA treatment reduces the sensitivity to the naloxone-precipitated withdrawal reaction, but does not affect the development of physical dependence.
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PMID:The influence of p-chlorophenylalanine on different morphine effects. 644 58

We aimed to elucidate the role of alpha(1)-adrenoceptors in adenosine analgesia in the formalin test. Formalin was injected into the hind paw of male CD-1 mice after injection of adenosine A(1) or A(2a) receptor agonists, CPA, [N(6)-cyclopentyladenosine], and CGS21680 [2-p-(2-carboxyethyl)-phenylethylamino-5'-N-ethylcarboxamidoadenosine hydrochloride]. In the behavioral experiment, alpha(1)-adrenoceptors were blocked by an alpha(1)-adrenoceptor antagonist prazosin, 0.01 mg/kg i.p., and the time mice spent paw licking was recorded for the early (0-15 min) and late (15-60 min) phase of formalin pain. In the neurochemical experiments, mice were killed 15 or 45 min after formalin injection. The density of alpha(1)-adrenoceptors was assessed in various brain areas and in the lumbar spinal cord by [(3)H]prazosin autoradiography. Adenosine agonists produced analgesia in both phases of formalin pain, while prazosin showed a tendency to pronociceptive action in the late phase, and antagonized the effect of CGS21680. After formalin injection, alpha(1)-adrenoceptor density was elevated in some brain areas, mainly in the late phase (some contralateral amygdaloid and ipsilateral thalamic nuclei) and depressed in others (early phase in the ipsilateral spinal cord and late phase in both ipsi- and contralateral sensorimotor cortex). Elevation of alpha(1)-adrenoceptor density, which may be interpreted as a defensive response, did not develop in several cases of CPA-pretreated mice. This suggests that the analgesic effect of adenosine A(1) receptor activation renders the defensive response unnecessary. The depression of alpha(1)-adrenoceptors may suggest development of hypersensitivity in a given structure, and this was antagonized by CGS21680, suggesting the role of A(2a) receptors in control of inflammatory formalin pain.
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PMID:Changes induced by formalin pain in central alpha1-adrenoceptor density are modulated by adenosine receptor agonists. 2030 90

The authors review the opioid literature for evidence of increased analgesia and reduced adverse side effects by combining mu-opioid-receptor (MOR) agonists, kappa-opioid-receptor (KOR) agonists, and nonselective low-dose-opioid antagonists (LD-Ant). We tested fentanyl (MOR agonist) and spiradoline (KOR agonist), singly and combined, against somatic and visceral pain models. Combined agonists induced additive analgesia in somatic pain and synergistic analgesia in visceral pain. Other investigators report similar effects and reduced tolerance and dependence with combined MOR agonist and KOR agonist. LD-Ant added to either a MOR agonist or KOR agonist markedly enhanced analgesia of either agonist. In accordance with other place-conditioning (PC) studies, our PC investigations showed fentanyl-induced place preference (CPP) and spiradoline-induced place aversion (CPA). We reduced fentanyl CPP with a low dose of spiradoline and reduced spiradoline CPA with a low dose of fentanyl. We propose combined MOR agonist, KOR agonist, and LD-Ant to produce superior analgesia with reduced adverse side effects, particularly for visceral pain.
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PMID:Effects of combined opioids on pain and mood in mammals. 2255 May 75