Several reasons why ketamine as a neuroplastic agent may have failed to prevent postoperative delirium: Implications for future protocols
Jazyk angličtina Země Irsko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
36693556
DOI
10.1016/j.neulet.2023.137095
PII: S0304-3940(23)00049-6
Knihovny.cz E-zdroje
- Klíčová slova
- Anesthesia, Benzodiazepines, Ketamine, Neuroplastic, Neuroprotective, Pharmacological interaction, Postoperative delirium,
- MeSH
- anestetika celková * MeSH
- anestetika disociativní MeSH
- anestetika intravenózní MeSH
- celková anestezie MeSH
- ketamin * terapeutické užití MeSH
- lidé MeSH
- pooperační delirium * farmakoterapie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- anestetika celková * MeSH
- anestetika disociativní MeSH
- anestetika intravenózní MeSH
- ketamin * MeSH
Ketamine exerts anti-inflammatory, neuroprotective and neuroplastic activity, therefore it may counteract the neurotoxic processes underlying postoperative delirium. However, the majority of studies in this field failed. We identified several pharmacological reasons why these studies may have failed, together with suggestions of how to remediate them. Among them, the interaction with intravenous general anesthetics exerting the opposite effect on GABA interneurons than ketamine may be of principal importance. We suggest biomarkers which may elucidate the influence of this interaction on the different steps of neuroplastic pathways. We hypothesize that administering ketamine before or after general anesthesia could both prevent the interactions and strengthen the effect of ketamine by timing surgery within the climax of ketamine-induced neuroplastic changes or by stabilizing AMPA receptors. It is vital to deal with these questions because the protocols of ongoing studies are based again on the administration of ketamine during general anesthesia (the major identified pitfall).
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