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)

Hemoglobin-(= Met-Hb)formation by local anaesthesia and local anaesthetics is still a point for discussion. Until now met-hb-aemia only was proven to develop under local anaesthetics with relationship to aniline (Benzocaine, Citanest). Since aniline does not possess any oxidative properties, met-hb-formation only can occur after metabolism (phenylhydroxylamine or para-aminophenol), first of all amino- and nitro-groups [6, 14] will be made responsible for oxidation. Because of the fact that neither the relationship to aniline nor the benzol-structure is the pre-supposition for met-hb-formation, possibly other substances with amino- or nitro-groups may induce it. In consequence of incidental cyanosis under intra and extradural analgesia we studied the met-hb-behaviour after the use of different local anaesthetics. The aniline-related bupivacaine and etidocaine were opposed to the thiophene-related carticaine. In this examination we found neither an elevation of hemoglobin by the aniline-related nor by the thiophene-related substances.
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PMID:[Met-Hb formation and local anesthesia using bupivacaine, carticaine and etidocaine (author's transl)]. 724 10

The influence of rifampicin on the toxicity, analgesic effect and pharmacokinetics of acetaminophen was studied in male albino mice. Repeated administration of rifampicin (50 mg/kg i.p. daily for 6 days) shortened hexobarbital sleeping time and increased liver weight, microsomal cytochrome P-450 and heme contents, NADPH-cytochrome c reductase and ethylmorphine-N-demethylase activities. Aniline hydroxylase activity was decreased and glucuronidation of p-nitrophenol was unaffected. Rifampicin pretreatment changed neither the LD50 of acetaminophen nor the hepatic glutathione level nor the glutathione depletion provoked by the toxic dose of acetaminophen (737 mg/kg p.o.). This suggests that rifampicin has no influence on the amount of acetaminophen toxic metabolites formed in the liver. Rifampicin decreased the acetaminophen analgesic effect in mice. Rifampicin decreased the Cmax, the half-time, the MRT and the AUC of acetaminophen and accelerated its clearance. The plasma concentration of acetaminophen glucuronide and acetaminophen sulfate was increased. It is assumed that the most probable mechanism by which rifampicin decreases acetaminophen analgesia is the accelerated acetaminophen elimination.
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PMID:Influence of rifampicin on the toxicity and the analgesic effect of acetaminophen. 773 32

The influence of long-term nifedipine administration on the antinociceptive activity of acetaminophen on hexobarbital sleeping time and liver monooxygenase and synthetase activities was studied in male albino mice. Nifedipine was administered orally at a dose of 25 mg/kg daily for 14 and 21 days. The nociceptive response was determined by the acetic acid writhing test. There was no significant difference in the antinociceptive effect of acetaminophen after treatment with nifedipine for 14 days. Nifedipine caused enzyme induction, which was demonstrated by shortened hexobarbital sleeping time, enhanced ethylmorphine-N-demethylase (EMND), aniline-4-hydroxylase (AH), ethoxycoumarine-O-deethylase (ECOD), UDP-glucuronyl transferase (UDPGT), glutathione-S-transferase (GST) and NADPH-cytochrome c reductase activity and increased content of cytochrome P450 and cytochrome b5. It is assumed that this effect of nifedipine on acetaminophen analgesia is associated with the changes (acceleration) in acetaminophen metabolism in the liver after repeated administration of the drug.
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PMID:Effect of long-term multiple nifedipine administration on the antinociceptive activity of acetaminophen. 1195 44