Literature DB >> 22692377

Estimation of the contribution of norketamine to ketamine-induced acute pain relief and neurocognitive impairment in healthy volunteers.

Erik Olofsen1, Ingeborg Noppers, Marieke Niesters, Evan Kharasch, Leon Aarts, Elise Sarton, Albert Dahan.   

Abstract

BACKGROUND: The N-methyl-D-aspartate receptor antagonist ketamine is metabolized in the liver into its active metabolite norketamine. No human data are available on the relative contribution of norketamine to ketamine-induced analgesia and side effects. One approach to assess the ketamine and norketamine contributions is by measuring the ketamine effect at varying ketamine and norketamine plasma concentrations using the CYP450 inducer rifampicin.
METHODS: In 12 healthy male volunteers the effect of rifampicin versus placebo pretreatment on S-ketamine-induced analgesia and cognition was quantified; the S-ketamine dosage was 20 mg/h for 2 h. The relative ketamine and norketamine contribution to effect was estimated using a linear additive population pharmacokinetic-pharmacodynamic model.
RESULTS: S-ketamine produced significant analgesia, psychotropic effects (drug high), and cognitive impairment (including memory impairment and reduced psychomotor speed, reaction time, and cognitive flexibility). Modeling revealed a negative contribution of S-norketamine to S-ketamine- induced analgesia and absence of contribution to cognitive impairment. At ketamine and norketamine effect concentrations of 100 ng/ml and 50 ng/ml, respectively, the ketamine contribution to analgesia is -3.8 cm (visual analog pain score) versus a contribution of norketamine of +1.5 cm, causing an overall effect of -2.3 cm. The blood-effect site equilibration half-life ranged from 0 (cognitive flexibility) to 11.8 (pain intensity) min and was 6.1 min averaged across all endpoints.
CONCLUSIONS: This first observation that norketamine produces effects in the opposite direction of ketamine requires additional proof. It can explain the observation of ketamine-related excitatory phenomena (such as hyperalgesia and allodynia) upon the termination of ketamine infusions.

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Year:  2012        PMID: 22692377      PMCID: PMC3406234          DOI: 10.1097/ALN.0b013e31825b6c91

Source DB:  PubMed          Journal:  Anesthesiology        ISSN: 0003-3022            Impact factor:   7.892


  29 in total

1.  Generalized hyperalgesia and allodynia following abrupt cessation of subcutaneous ketamine infusion.

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4.  Effect of ketamine on endogenous pain modulation in healthy volunteers.

Authors:  Marieke Niesters; Albert Dahan; Maarten Swartjes; Ingeborg Noppers; Roger B Fillingim; Leon Aarts; Elise Y Sarton
Journal:  Pain       Date:  2011-01-14       Impact factor: 6.961

5.  Nonselective and NR2B-selective N-methyl-D-aspartic acid receptor antagonists produce antinociception and long-term relief of allodynia in acute and neuropathic pain.

Authors:  Maarten Swartjes; Aurora Morariu; Marieke Niesters; Leon Aarts; Albert Dahan
Journal:  Anesthesiology       Date:  2011-07       Impact factor: 7.892

6.  Effect of rifampicin on S-ketamine and S-norketamine plasma concentrations in healthy volunteers after intravenous S-ketamine administration.

Authors:  Ingeborg Noppers; Erik Olofsen; Marieke Niesters; Leon Aarts; René Mooren; Albert Dahan; Evan Kharasch; Elise Sarton
Journal:  Anesthesiology       Date:  2011-06       Impact factor: 7.892

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10.  An observational study on the effect of S+-ketamine on chronic pain versus experimental acute pain in Complex Regional Pain Syndrome type 1 patients.

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7.  Predictive performance of parent-metabolite population pharmacokinetic models of (S)-ketamine in healthy volunteers.

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