Forebrain Ischemia-Reperfusion Simulating Cardiac Arrest in Mice Induces Edema and DNA Fragmentation in the Brain

Brain injury affects one-third of persons who survive after heart attack, even with restoration of spontaneous circulation by cardiopulmonary resuscitation. We studied brain injury resulting from transient bilateral carotid artery occlusion (BCAO) and reperfusion by simulating heart attack and resto...

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Main Authors: Christina H. Liu, Shuning Huang, Young R. Kim, Bruce R. Rosen, Philip K. Liu
Format: Article
Language:English
Published: SAGE Publishing 2007-05-01
Series:Molecular Imaging
Online Access:https://doi.org/10.2310/7290.2007.00011
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author Christina H. Liu
Shuning Huang
Young R. Kim
Bruce R. Rosen
Philip K. Liu
author_facet Christina H. Liu
Shuning Huang
Young R. Kim
Bruce R. Rosen
Philip K. Liu
author_sort Christina H. Liu
collection DOAJ
description Brain injury affects one-third of persons who survive after heart attack, even with restoration of spontaneous circulation by cardiopulmonary resuscitation. We studied brain injury resulting from transient bilateral carotid artery occlusion (BCAO) and reperfusion by simulating heart attack and restoration of circulation, respectively, in live C57Black6 mice. This model is known to induce neuronal death in the hippocampus, striatum, and cortex. We report the appearance of edema after transient BCAO of 60 minutes and 1 day of reperfusion. Hyperintensity in diffusion-weighted magnetic resonance imaging (MRI) was detectable in the striatum, thalamus, and cortex but not in the hippocampus. To determine whether damage to the hippocampus can be detected in live animals, we infused a T 2 susceptibility magnetic resonance contrast agent (superparamagnetic iron oxide nanoparticles [SPIONs]) that was linked to single-stranded deoxyribonucleic acid (DNA) complementary in sequence to c-fos messenger ribonucleic acid (SPION-cfos); we acquired in vivo T 2 * -weighted MRI 3 days later. SPION retention was measured as T 2 * (milliseconds) signal reduction or R 2 * value (s −1 ) elevation. We found that animals treated with 60-minute BCAO and 7-day reperfusion exhibited significantly less SPION retention in the hippocampus and cortex than sham-operated animals. These findings suggest that brain injury induced by cardiac arrest can be detected in live animals.
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spelling doaj-art-2d1dd6486c6f4632aaaf067de6cd52cf2025-01-02T23:12:07ZengSAGE PublishingMolecular Imaging1536-01212007-05-01610.2310/7290.2007.0001110.2310_7290.2007.00011Forebrain Ischemia-Reperfusion Simulating Cardiac Arrest in Mice Induces Edema and DNA Fragmentation in the BrainChristina H. LiuShuning HuangYoung R. KimBruce R. RosenPhilip K. LiuBrain injury affects one-third of persons who survive after heart attack, even with restoration of spontaneous circulation by cardiopulmonary resuscitation. We studied brain injury resulting from transient bilateral carotid artery occlusion (BCAO) and reperfusion by simulating heart attack and restoration of circulation, respectively, in live C57Black6 mice. This model is known to induce neuronal death in the hippocampus, striatum, and cortex. We report the appearance of edema after transient BCAO of 60 minutes and 1 day of reperfusion. Hyperintensity in diffusion-weighted magnetic resonance imaging (MRI) was detectable in the striatum, thalamus, and cortex but not in the hippocampus. To determine whether damage to the hippocampus can be detected in live animals, we infused a T 2 susceptibility magnetic resonance contrast agent (superparamagnetic iron oxide nanoparticles [SPIONs]) that was linked to single-stranded deoxyribonucleic acid (DNA) complementary in sequence to c-fos messenger ribonucleic acid (SPION-cfos); we acquired in vivo T 2 * -weighted MRI 3 days later. SPION retention was measured as T 2 * (milliseconds) signal reduction or R 2 * value (s −1 ) elevation. We found that animals treated with 60-minute BCAO and 7-day reperfusion exhibited significantly less SPION retention in the hippocampus and cortex than sham-operated animals. These findings suggest that brain injury induced by cardiac arrest can be detected in live animals.https://doi.org/10.2310/7290.2007.00011
spellingShingle Christina H. Liu
Shuning Huang
Young R. Kim
Bruce R. Rosen
Philip K. Liu
Forebrain Ischemia-Reperfusion Simulating Cardiac Arrest in Mice Induces Edema and DNA Fragmentation in the Brain
Molecular Imaging
title Forebrain Ischemia-Reperfusion Simulating Cardiac Arrest in Mice Induces Edema and DNA Fragmentation in the Brain
title_full Forebrain Ischemia-Reperfusion Simulating Cardiac Arrest in Mice Induces Edema and DNA Fragmentation in the Brain
title_fullStr Forebrain Ischemia-Reperfusion Simulating Cardiac Arrest in Mice Induces Edema and DNA Fragmentation in the Brain
title_full_unstemmed Forebrain Ischemia-Reperfusion Simulating Cardiac Arrest in Mice Induces Edema and DNA Fragmentation in the Brain
title_short Forebrain Ischemia-Reperfusion Simulating Cardiac Arrest in Mice Induces Edema and DNA Fragmentation in the Brain
title_sort forebrain ischemia reperfusion simulating cardiac arrest in mice induces edema and dna fragmentation in the brain
url https://doi.org/10.2310/7290.2007.00011
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