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

The incidence of retention of urine in cases of postoperative epidural opioid analgesia varies from 15% to 90%. The extent to which this phenomenon depends upon the dosage employed has not been elucidated. The cause of postoperative retention of urine (PU) is probably a combination of the central and peripheral effect of the opiate involving altered autonomic activity. Increased sympathetic activity resulting from surgery may, similarly, be a pathogenetic factor. The current methods of treatment are prophylactic or symptomatic alpha-receptor blockade, naloxon in refractory doses or catheterization. Inhibition of per- and postoperatively increased sympathetic activity may possibly prevent PU. Carbacholine is not effective in the treatment of postoperative retention of urine. In animal experimental studies, kappa-receptor agonists have an analgesic effect without urodynamic side-effects but no clinical trials on man have hitherto been undertaken. When postoperative retention of urine occurs after epidural opioid treatment, clean intermittent catheterization or introduction of a thin suprapubic catheter are recommended.
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PMID:[Urinary retention in connection with postoperative pain treatment with epidural opioids]. 219 50

The amplitude of vocalization and the motor defense response evoked by painful electrical stimulation were recorded in unanesthetized guinea pigs submitted to topical application of 1.0 microgram/microliter carbachol to the area postrema. Carbachol was found to have an analgesic effect. A similar application of 3.0 micrograms/microliter 5-hydroxytryptamine (5-HT) also had an analgesic effect, whose duration, however, was only half that of carbachol and whose intensity was lower, although the latency of the response was 2 seconds for both drugs. When 100 micrograms/microliter lysergic acid was applied to the area postrema the results did not differ significantly from control values, with only a small tendency toward hyperalgesia being observed. The present results, taken together with those obtained with noradrenalin in a previous study, suggest that the rich endowment of neurotransmitters in the area postrema may indicate a polyvalent analgesic mechanism able to provide a finer regulation of analgesia.
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PMID:Inhibition of the response to pain by the action of serotonin and carbachol topically applied to the area postrema of conscious guinea pigs. 406 51

These studies investigated the effect of microinjection of the cholinergic agonist carbamylcholine (carbachol) into various sites of the dorsolateral pontine tegmentum of the cat. Carbachol microinjection into an area surrounding the lateral half of the brachium conjunctivum (parabrachial region, PBR) produced profound suppression of nociceptive responses. In the dorsal part of PBR, carbachol microinjection produced no generalized sensory, emotional or motor deficits, indicating that nociceptive transmission was primarily affected. Carbachol microinjection into the ventral part of PBR resulted in slight suppression of motor responses in addition to profound nociceptive suppression. Carbachol-produced analgesia (CPA) observed within PBR blocked supraspinally as well as spinally integrated responses normally elicited by either phasic or tonic noxious stimuli. Atropine sulfate, but not mecamylamine hydrochloride, significantly antagonized CPA, indicating that muscarinic receptors mediate this phenomenon. The opiate antagonist naloxone, systemically administered either prior to or after carbachol microinjection, did not reliably attenuate CPA. Microinjection of morphine into the sites from which CPA had previously been obtained did not produce significant effects on nociceptive responses. Thus, opiate mechanisms appear not to be necessary either for the activation of this system or for the production of the resultant analgesia. These findings indicate that the neural population examined in the present study is anatomically and pharmacologically distinct from previously identified opiate-mediated pain inhibitory systems. Results are discussed in light of other recent evidence indicating the existence of endogenous non-opiate pain inhibitory systems.
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PMID:Non-opiate analgesia induced by carbachol microinjection into the pontine parabrachial region of the cat. 632 25

The Hippocampus has a role not only in nociception but also in modulation of pain perception. In addition, orexinergic neurons present in the lateral hypothalamus (LH) have a recognized role in pain modulation. The presence of orexinergic projections from the lateral hypothalamus (LH) to the dorsal hippocampal Cornu Ammonis 1 (CA1) region raises the question of whether pain modulatory role of LH is mediated through the CA1. To elucidate the interactions between the LH and neural substrates involved in modulation of formalin-induced nociception, the study aimed to test the pain modulatory role of CA1 orexin receptors in the formalin test. Seventy-one male Wistar rats were unilaterally implanted with two cannulae above the LH and CA1. In the treatment groups, intra-CA1 administration of SB-334867, as an orexin-1 receptor antagonist, was performed 5min before intra-LH microinjection of carbachol, as a cholinergic receptor agonist. In dimethyl sulfoxide (DMSO)-control group, DMSO and saline as well as in carbachol-control group, DMSO and carbachol were microinjected into the CA1 and LH, respectively. In all rats, the procedure was followed by subcutaneous injection of formalin after 5-min time interval. Carbachol reduced both phases of formalin-induced nociception. Intra-CA1 administration of SB-334867 antagonized the LH-induced analgesia during both phases in a dose-dependent manner. It seems that the blockade of orexin-1 receptors has more effects on reduction of antinociception during the late phase compared to the early phase. Pain modulatory role of orexinergic system in the formalin test through a neural pathway from the LH to CA1 provides the evidence that orexins can be useful therapeutic agents for chronic pain treatment.
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PMID:Role of dorsal hippocampal orexin-1 receptors in modulation of antinociception induced by chemical stimulation of the lateral hypothalamus. 2929 5

The lateral hypothalamus (LH) plays a complicated role in the modulation of inflammatory pain. There are a number of connections between the LH and the hippocampus. This study evaluated the pain modulatory role of intra-CA1 dopamine receptors in LH chemical stimulation-induced antinociception in the formalin test (persistent inflammatory pain model). Vehicle control groups received saline or DMSO into the CA1 and saline into the LH. Carbachol control groups received carbachol (250 nM) into the LH 5 min after saline or DMSO injections into the CA1. In the treatment groups, intra-CA1 administration of SCH-23,390 or Sulpiride (D1- or D2-like dopamine receptor antagonists, respectively) was performed 5 min before carbachol injection. Formalin tests were done in all rats 5 min after the second injection. LH chemical stimulation-induced antinociception during both phases of the formalin test was alleviated by the intra-CA1 administration of dopamine receptor antagonists. The inhibitory effects of the D1 or D2-like dopamine receptor antagonist on LH chemical stimulation-induced analgesia was nearly the same in the both phases of formalin-induced pain-related behaviors. The findings show that the LH-CA1 pathway contributes to the modulation of formalin-induced pain. Moreover, the results indicate that D1- and D2-like dopamine receptors in the CA1 participate in the LH chemical stimulation-induced antinociception.
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PMID:Modulatory role of hippocampal dopamine receptors in antinociceptive responses induced by chemical stimulation of the lateral hypothalamus in an animal model of persistent inflammatory pain. 3261 58