Preclinical Positron Emission Tomographic Imaging of Acute Hyperoxia Therapy of Chronic Hypoxia during Pregnancy

The goal of this work was to study the efficacy of the positron emission tomography (PET) tracers 2-deoxy-2-[ 18 F]fluoro-D-glucose ([ 18 F]FDG) and 64 Cu-diacetyl-bis(N4-methylthiosemicarbazone) ([ 64 Cu]ATSM) and in monitoring placental and fetal functional response to acute hyperoxia in late-term...

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Main Authors: Alexander Zheleznyak, Joel R. Garbow, Michal Neeman, Suzanne E. Lapi
Format: Article
Language:English
Published: SAGE Publishing 2015-07-01
Series:Molecular Imaging
Online Access:https://doi.org/10.2310/7290.2015.00013
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author Alexander Zheleznyak
Joel R. Garbow
Michal Neeman
Suzanne E. Lapi
author_facet Alexander Zheleznyak
Joel R. Garbow
Michal Neeman
Suzanne E. Lapi
author_sort Alexander Zheleznyak
collection DOAJ
description The goal of this work was to study the efficacy of the positron emission tomography (PET) tracers 2-deoxy-2-[ 18 F]fluoro-D-glucose ([ 18 F]FDG) and 64 Cu-diacetyl-bis(N4-methylthiosemicarbazone) ([ 64 Cu]ATSM) and in monitoring placental and fetal functional response to acute hyperoxia in late-term pregnant mice subjected to experimentally induced chronic hypoxia. E15 mice were maintained at 12% inspired oxygen for 72 hours and then imaged during oxygen inhalation with either [ 18 F]FDG to monitor nutrient transport or 64 Cu-ATSM to establish the presence of hypoxia. Computed tomography (CT) with contrast allowed clear visualization of both placentas and fetuses. The average ratio of fetal to placental [ 18 F]FDG uptake was 0.45 ± 0.1 for the hypoxic animals and 0.55 ± 0.1 for the normoxic animals, demonstrating a significant decrease ( p = .0002) in placental function in dams exposed to chronic hypoxic conditions. Hypoxic placentas and fetuses retained more 64 Cu-ATSM compared to normoxic placentas and fetuses. Herein we report first-in-mouse PET imaging of fetuses employing both tracers [ 18 F]FDG (metabolism) and 64 Cu-ATSM (hypoxia). [ 18 F]FDG PET/CT imaging allowed clear visualization of placental-fetal structures and supported quantification of tracer uptake, making this a sensitive tool for monitoring placental function in preclinical rodent models. These measurements illustrate the potentially irreversible damage generated by chronic exposure to hypoxia, which cannot be corrected by acute exposure to hyperoxia.
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spelling doaj-art-0f72b3b9d812409b9f24d897a4bc83992025-02-03T10:07:51ZengSAGE PublishingMolecular Imaging1536-01212015-07-011410.2310/7290.2015.0001310.2310_7290.2015.00013Preclinical Positron Emission Tomographic Imaging of Acute Hyperoxia Therapy of Chronic Hypoxia during PregnancyAlexander ZheleznyakJoel R. GarbowMichal NeemanSuzanne E. LapiThe goal of this work was to study the efficacy of the positron emission tomography (PET) tracers 2-deoxy-2-[ 18 F]fluoro-D-glucose ([ 18 F]FDG) and 64 Cu-diacetyl-bis(N4-methylthiosemicarbazone) ([ 64 Cu]ATSM) and in monitoring placental and fetal functional response to acute hyperoxia in late-term pregnant mice subjected to experimentally induced chronic hypoxia. E15 mice were maintained at 12% inspired oxygen for 72 hours and then imaged during oxygen inhalation with either [ 18 F]FDG to monitor nutrient transport or 64 Cu-ATSM to establish the presence of hypoxia. Computed tomography (CT) with contrast allowed clear visualization of both placentas and fetuses. The average ratio of fetal to placental [ 18 F]FDG uptake was 0.45 ± 0.1 for the hypoxic animals and 0.55 ± 0.1 for the normoxic animals, demonstrating a significant decrease ( p = .0002) in placental function in dams exposed to chronic hypoxic conditions. Hypoxic placentas and fetuses retained more 64 Cu-ATSM compared to normoxic placentas and fetuses. Herein we report first-in-mouse PET imaging of fetuses employing both tracers [ 18 F]FDG (metabolism) and 64 Cu-ATSM (hypoxia). [ 18 F]FDG PET/CT imaging allowed clear visualization of placental-fetal structures and supported quantification of tracer uptake, making this a sensitive tool for monitoring placental function in preclinical rodent models. These measurements illustrate the potentially irreversible damage generated by chronic exposure to hypoxia, which cannot be corrected by acute exposure to hyperoxia.https://doi.org/10.2310/7290.2015.00013
spellingShingle Alexander Zheleznyak
Joel R. Garbow
Michal Neeman
Suzanne E. Lapi
Preclinical Positron Emission Tomographic Imaging of Acute Hyperoxia Therapy of Chronic Hypoxia during Pregnancy
Molecular Imaging
title Preclinical Positron Emission Tomographic Imaging of Acute Hyperoxia Therapy of Chronic Hypoxia during Pregnancy
title_full Preclinical Positron Emission Tomographic Imaging of Acute Hyperoxia Therapy of Chronic Hypoxia during Pregnancy
title_fullStr Preclinical Positron Emission Tomographic Imaging of Acute Hyperoxia Therapy of Chronic Hypoxia during Pregnancy
title_full_unstemmed Preclinical Positron Emission Tomographic Imaging of Acute Hyperoxia Therapy of Chronic Hypoxia during Pregnancy
title_short Preclinical Positron Emission Tomographic Imaging of Acute Hyperoxia Therapy of Chronic Hypoxia during Pregnancy
title_sort preclinical positron emission tomographic imaging of acute hyperoxia therapy of chronic hypoxia during pregnancy
url https://doi.org/10.2310/7290.2015.00013
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