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)

Several interventions have been demonstrated, with high evidence levels (EL), to be associated with reduced instrumental deliveries and should therefore be undertaken during labor for increasing spontaneous vaginal deliveries. Using a partogram (EL1) and continuous support during labor and childbirth (EL1) lead to fewer operative vaginal deliveries. Systematic early amniotomy increases the frequency of fetal heart rate abnormalities (EL2) without decreasing the incidence of instrumental deliveries (EL1) and should thus be avoided. Early oxytocin in dysfunctional labor (EL2) and manual rotation of posterior and transverse presentations (EL3) may reduce operative vaginal deliveries. Even without epidural analgesia, any upright or lateral positions compared to supine or lithotomy positions do not reduce instrumental deliveries (EL2). Epidural analgesia alters significantly instrumental delivery rates and therefore patient management in the labor ward. Indeed, when used with high concentration of local anesthetic, epidural analgesia is associated with increased operative vaginal deliveries (EL1), at least in part because of increased posterior presentations (EL2). However, the effect of epidural analgesia on instrumental delivery rates closely depends from the type of anesthetic and concentrations used. This effect is reduced when low concentrations of local anesthetic are used in combination with fat-soluble morphinated agent (EL1). Finally, for nulliparous women with continuous epidural analgesia, unless irresistible urge to push or medical indication to shorten second stage of labor, delayed pushing is associated with reduced difficult instrumental deliveries (EL1). Fundal pressure maneuvers should be prohibited because of their inefficiency (EL2) and dangerousness (EL4).
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PMID:[Interventions during labor for reducing instrumental deliveries]. 1926 95

This study searched for polymorphic sites in the murine mu-, delta- and kappa-opioid receptors that presumably influence pain perception. We employed two mouse lines divergently bred for high (HA, high analgesia line) and low (LA, low analgesia line) swim stress-induced analgesia (SSIA). These mouse lines differ substantially in pain sensitivity, measured as hind paw withdrawal latency in the hot-plate test. We found a novel C320T transition in exon 2 of the delta-opioid receptor gene, resulting in an A107V substitution in the first extracellular loop (EL1) of the peptide chain. Using hot-plate and tail-flick tests, we found a significant association between the genotype of this locus and basal nociception and SSIA magnitude. Moreover, this transition affects the pharmacological effects of two specific delta-opioid receptor ligands, the agonist SNC80 and the antagonist naltrindole. The impact of the C320T polymorphism on the magnitude of SSIA was partially mediated by endogenous opioids. The effectiveness of exogenous delta-opioid receptor ligands was greater in the HA than in the LA line, and was greater in C320C homozygotes than in C320T heterozygotes within each line. Our results indicate that the C320T polymorphism in the delta-opioid receptor gene is at least partly responsible for the divergent nociceptive thresholds in HA and LA mice under both basal and post-stress conditions.
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PMID:A polymorphism in exon 2 of the delta-opioid receptor affects nociception in response to specific agonists and antagonists in mice selectively bred for high and low analgesia. 2038 Dec 45