Reduced oxycodone brain delivery in rats due to lipopolysaccharide-induced inflammation: microdialysis insights into brain disposition and sex-specific pharmacokinetics

Abstract Background Oxycodone, a widely used opioid analgesic, has an unbound brain-to-plasma concentration ratio (Kp,uu) greater than unity, indicating active uptake across brain barriers associated with the putative proton-coupled organic cation (H+/OC) antiporter system. With this study, we aimed...

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Main Authors: Frida Bällgren, Margareta Hammarlund-Udenaes, Irena Loryan
Format: Article
Language:English
Published: BMC 2024-12-01
Series:Fluids and Barriers of the CNS
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Online Access:https://doi.org/10.1186/s12987-024-00598-6
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author Frida Bällgren
Margareta Hammarlund-Udenaes
Irena Loryan
author_facet Frida Bällgren
Margareta Hammarlund-Udenaes
Irena Loryan
author_sort Frida Bällgren
collection DOAJ
description Abstract Background Oxycodone, a widely used opioid analgesic, has an unbound brain-to-plasma concentration ratio (Kp,uu) greater than unity, indicating active uptake across brain barriers associated with the putative proton-coupled organic cation (H+/OC) antiporter system. With this study, we aimed to elucidate oxycodone's CNS disposition during lipopolysaccharide (LPS)-induced systemic inflammation in Sprague–Dawley rats. Methods Using brain microdialysis, we dynamically and simultaneously monitored unbound oxycodone concentrations in blood, striatum, lateral ventricle, and cisterna magna following intravenous administration of oxycodone post-LPS challenge. Results Our results indicated a reduced, sex-independent brain net uptake of oxycodone across the blood–brain barrier (BBB) measured in the striatum. Notably, the LPS challenge has significantly altered the systemic pharmacokinetics (PK) of oxycodone, in a sex-specific manner, leading to lower clearance and higher blood concentrations in females compared to LPS-treated males and healthy rats of both sexes. Proteomic analysis using Olink Target 96 Mouse Exploratory assay confirmed the induction of systemic inflammation and neuroinflammation. The inflammation led to an increased paracellular transport, measured using 4 kDa dextran, while preserving net active uptake of oxycodone across both BBB and the blood-cerebrospinal fluid barrier (BCSFB), with Kp,uu values of 2.7 and 2.5, respectively. The extent of uptake was 1.6-fold lower (p < 0.0001) at the BBB and unchanged at the BCSFB after the LPS challenge compared to that in healthy rats. However, the mean exposure of unbound oxycodone in the brain following LPS was similar to that in healthy rats, primarily due to the LPS-induced changes in systemic exposure. Conclusions These findings highlight the dissimilar responses at blood–brain interfaces during LPS-induced inflammation. Advancing the knowledge of neuropharmacokinetic mechanisms, specifically those involving the H+/OC antiporter system, will enable the development of more effective therapeutic strategies during inflammation conditions. Graphical Abstract
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spelling doaj-art-4ecdbedc52f547b4854d4f0f4ccd66d32024-12-08T12:41:40ZengBMCFluids and Barriers of the CNS2045-81182024-12-0121111810.1186/s12987-024-00598-6Reduced oxycodone brain delivery in rats due to lipopolysaccharide-induced inflammation: microdialysis insights into brain disposition and sex-specific pharmacokineticsFrida Bällgren0Margareta Hammarlund-Udenaes1Irena Loryan2Translational Pharmacokinetics/Pharmacodynamics Group (tPKPD), Department of Pharmacy, Uppsala UniversityTranslational Pharmacokinetics/Pharmacodynamics Group (tPKPD), Department of Pharmacy, Uppsala UniversityTranslational Pharmacokinetics/Pharmacodynamics Group (tPKPD), Department of Pharmacy, Uppsala UniversityAbstract Background Oxycodone, a widely used opioid analgesic, has an unbound brain-to-plasma concentration ratio (Kp,uu) greater than unity, indicating active uptake across brain barriers associated with the putative proton-coupled organic cation (H+/OC) antiporter system. With this study, we aimed to elucidate oxycodone's CNS disposition during lipopolysaccharide (LPS)-induced systemic inflammation in Sprague–Dawley rats. Methods Using brain microdialysis, we dynamically and simultaneously monitored unbound oxycodone concentrations in blood, striatum, lateral ventricle, and cisterna magna following intravenous administration of oxycodone post-LPS challenge. Results Our results indicated a reduced, sex-independent brain net uptake of oxycodone across the blood–brain barrier (BBB) measured in the striatum. Notably, the LPS challenge has significantly altered the systemic pharmacokinetics (PK) of oxycodone, in a sex-specific manner, leading to lower clearance and higher blood concentrations in females compared to LPS-treated males and healthy rats of both sexes. Proteomic analysis using Olink Target 96 Mouse Exploratory assay confirmed the induction of systemic inflammation and neuroinflammation. The inflammation led to an increased paracellular transport, measured using 4 kDa dextran, while preserving net active uptake of oxycodone across both BBB and the blood-cerebrospinal fluid barrier (BCSFB), with Kp,uu values of 2.7 and 2.5, respectively. The extent of uptake was 1.6-fold lower (p < 0.0001) at the BBB and unchanged at the BCSFB after the LPS challenge compared to that in healthy rats. However, the mean exposure of unbound oxycodone in the brain following LPS was similar to that in healthy rats, primarily due to the LPS-induced changes in systemic exposure. Conclusions These findings highlight the dissimilar responses at blood–brain interfaces during LPS-induced inflammation. Advancing the knowledge of neuropharmacokinetic mechanisms, specifically those involving the H+/OC antiporter system, will enable the development of more effective therapeutic strategies during inflammation conditions. Graphical Abstracthttps://doi.org/10.1186/s12987-024-00598-6Blood–brain barrierBlood-cerebrospinal fluid barrierOxycodoneMicrodialysisSexProton-coupled organic cation (H+/OC) antiporter
spellingShingle Frida Bällgren
Margareta Hammarlund-Udenaes
Irena Loryan
Reduced oxycodone brain delivery in rats due to lipopolysaccharide-induced inflammation: microdialysis insights into brain disposition and sex-specific pharmacokinetics
Fluids and Barriers of the CNS
Blood–brain barrier
Blood-cerebrospinal fluid barrier
Oxycodone
Microdialysis
Sex
Proton-coupled organic cation (H+/OC) antiporter
title Reduced oxycodone brain delivery in rats due to lipopolysaccharide-induced inflammation: microdialysis insights into brain disposition and sex-specific pharmacokinetics
title_full Reduced oxycodone brain delivery in rats due to lipopolysaccharide-induced inflammation: microdialysis insights into brain disposition and sex-specific pharmacokinetics
title_fullStr Reduced oxycodone brain delivery in rats due to lipopolysaccharide-induced inflammation: microdialysis insights into brain disposition and sex-specific pharmacokinetics
title_full_unstemmed Reduced oxycodone brain delivery in rats due to lipopolysaccharide-induced inflammation: microdialysis insights into brain disposition and sex-specific pharmacokinetics
title_short Reduced oxycodone brain delivery in rats due to lipopolysaccharide-induced inflammation: microdialysis insights into brain disposition and sex-specific pharmacokinetics
title_sort reduced oxycodone brain delivery in rats due to lipopolysaccharide induced inflammation microdialysis insights into brain disposition and sex specific pharmacokinetics
topic Blood–brain barrier
Blood-cerebrospinal fluid barrier
Oxycodone
Microdialysis
Sex
Proton-coupled organic cation (H+/OC) antiporter
url https://doi.org/10.1186/s12987-024-00598-6
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AT irenaloryan reducedoxycodonebraindeliveryinratsduetolipopolysaccharideinducedinflammationmicrodialysisinsightsintobraindispositionandsexspecificpharmacokinetics