Neurologic Deficit Score at 4–5 Days Post-eCPR Predicts Long-Term Brain Dysfunction in Rats Following Cardiac Arrest

Cardiac arrest (CA) survivors often develop long-term neurological deficits, but its long-term impact on vulnerable brain regions and neurological outcomes remains unclear. In a previous CA model with conventional cardiopulmonary resuscitation, we found reduced heme oxygenase (HO) activity in the hi...

Full description

Saved in:
Bibliographic Details
Main Authors: Wolfgang Weihs, Alexandra-Maria Stommel, Andrea Müllebner, Alexander Franz Szinovatz, Matthias Müller, Ingrid Magnet, Michael Holzer, Andrey V. Kozlov, Sandra Högler, J. Catharina Duvigneau
Format: Article
Language:English
Published: MDPI AG 2025-05-01
Series:Biomolecules
Subjects:
Online Access:https://www.mdpi.com/2218-273X/15/5/732
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850127627816271872
author Wolfgang Weihs
Alexandra-Maria Stommel
Andrea Müllebner
Alexander Franz Szinovatz
Matthias Müller
Ingrid Magnet
Michael Holzer
Andrey V. Kozlov
Sandra Högler
J. Catharina Duvigneau
author_facet Wolfgang Weihs
Alexandra-Maria Stommel
Andrea Müllebner
Alexander Franz Szinovatz
Matthias Müller
Ingrid Magnet
Michael Holzer
Andrey V. Kozlov
Sandra Högler
J. Catharina Duvigneau
author_sort Wolfgang Weihs
collection DOAJ
description Cardiac arrest (CA) survivors often develop long-term neurological deficits, but its long-term impact on vulnerable brain regions and neurological outcomes remains unclear. In a previous CA model with conventional cardiopulmonary resuscitation, we found reduced heme oxygenase (HO) activity in the hippocampus and cortex 14 days post-CA, suggesting its potential as a functional outcome marker. Here, we used a rat model with 6 or 8 min of CA followed by extracorporeal cardiopulmonary resuscitation. While in the 6 min-CA group, 67% survived to day 14, increased mortality within 4 days resulted in only 33% survival in the 8 min group post-ROSC. All animals displayed neurological impairment assessed by daily neurologic deficit scoring (NDS). While deficits declined within the first 3–4 days in the 6 min-CA animals, the 8 min-CA group showed significantly worse neurological outcomes until day 14. Two weeks post-CA, neuroinflammatory and neurodegenerative markers (HO-1, TNF-R1, Iba1, and GFAP) were elevated in the hippocampus, while HO and 2-oxoglutarate dehydrogenase complex activities were reduced in all rats, indicating a decrease in anti-oxidative capacity and mitochondrial capacity for metabolizing glutamate. NDS at day 4–5 strongly correlated with the delayed CA-mediated enzymatic dysfunction determined in the hippocampus. This finding highlights this time point for identifying at-risk individuals and suggests a prolonged therapeutic intervention lasting at least until 4 days post-CA.
format Article
id doaj-art-8875e929c69b473b8b06dfedb3aeb02e
institution OA Journals
issn 2218-273X
language English
publishDate 2025-05-01
publisher MDPI AG
record_format Article
series Biomolecules
spelling doaj-art-8875e929c69b473b8b06dfedb3aeb02e2025-08-20T02:33:38ZengMDPI AGBiomolecules2218-273X2025-05-0115573210.3390/biom15050732Neurologic Deficit Score at 4–5 Days Post-eCPR Predicts Long-Term Brain Dysfunction in Rats Following Cardiac ArrestWolfgang Weihs0Alexandra-Maria Stommel1Andrea Müllebner2Alexander Franz Szinovatz3Matthias Müller4Ingrid Magnet5Michael Holzer6Andrey V. Kozlov7Sandra Högler8J. Catharina Duvigneau9Department of Emergency Medicine, Medical University of Vienna, 1090 Vienna, AustriaDepartment of Emergency Medicine, Medical University of Vienna, 1090 Vienna, AustriaBiological Sciences and Pathobiology, University of Veterinary Medicine Vienna, 1221 Vienna, AustriaDepartment of Emergency Medicine, Medical University of Vienna, 1090 Vienna, AustriaDepartment of Emergency Medicine, Medical University of Vienna, 1090 Vienna, AustriaDepartment of Emergency Medicine, Medical University of Vienna, 1090 Vienna, AustriaDepartment of Emergency Medicine, Medical University of Vienna, 1090 Vienna, AustriaLudwig Boltzmann Institute for Traumatology, Research Center in Cooperation with AUVA, Austrian Cluster for Tissue Regeneration, 1200 Vienna, AustriaBiological Sciences and Pathobiology, University of Veterinary Medicine Vienna, 1221 Vienna, AustriaBiological Sciences and Pathobiology, University of Veterinary Medicine Vienna, 1221 Vienna, AustriaCardiac arrest (CA) survivors often develop long-term neurological deficits, but its long-term impact on vulnerable brain regions and neurological outcomes remains unclear. In a previous CA model with conventional cardiopulmonary resuscitation, we found reduced heme oxygenase (HO) activity in the hippocampus and cortex 14 days post-CA, suggesting its potential as a functional outcome marker. Here, we used a rat model with 6 or 8 min of CA followed by extracorporeal cardiopulmonary resuscitation. While in the 6 min-CA group, 67% survived to day 14, increased mortality within 4 days resulted in only 33% survival in the 8 min group post-ROSC. All animals displayed neurological impairment assessed by daily neurologic deficit scoring (NDS). While deficits declined within the first 3–4 days in the 6 min-CA animals, the 8 min-CA group showed significantly worse neurological outcomes until day 14. Two weeks post-CA, neuroinflammatory and neurodegenerative markers (HO-1, TNF-R1, Iba1, and GFAP) were elevated in the hippocampus, while HO and 2-oxoglutarate dehydrogenase complex activities were reduced in all rats, indicating a decrease in anti-oxidative capacity and mitochondrial capacity for metabolizing glutamate. NDS at day 4–5 strongly correlated with the delayed CA-mediated enzymatic dysfunction determined in the hippocampus. This finding highlights this time point for identifying at-risk individuals and suggests a prolonged therapeutic intervention lasting at least until 4 days post-CA.https://www.mdpi.com/2218-273X/15/5/732rat modelventricular fibrillation cardiac arresthippocampuscortexneurodegenerationheme oxygenase
spellingShingle Wolfgang Weihs
Alexandra-Maria Stommel
Andrea Müllebner
Alexander Franz Szinovatz
Matthias Müller
Ingrid Magnet
Michael Holzer
Andrey V. Kozlov
Sandra Högler
J. Catharina Duvigneau
Neurologic Deficit Score at 4–5 Days Post-eCPR Predicts Long-Term Brain Dysfunction in Rats Following Cardiac Arrest
Biomolecules
rat model
ventricular fibrillation cardiac arrest
hippocampus
cortex
neurodegeneration
heme oxygenase
title Neurologic Deficit Score at 4–5 Days Post-eCPR Predicts Long-Term Brain Dysfunction in Rats Following Cardiac Arrest
title_full Neurologic Deficit Score at 4–5 Days Post-eCPR Predicts Long-Term Brain Dysfunction in Rats Following Cardiac Arrest
title_fullStr Neurologic Deficit Score at 4–5 Days Post-eCPR Predicts Long-Term Brain Dysfunction in Rats Following Cardiac Arrest
title_full_unstemmed Neurologic Deficit Score at 4–5 Days Post-eCPR Predicts Long-Term Brain Dysfunction in Rats Following Cardiac Arrest
title_short Neurologic Deficit Score at 4–5 Days Post-eCPR Predicts Long-Term Brain Dysfunction in Rats Following Cardiac Arrest
title_sort neurologic deficit score at 4 5 days post ecpr predicts long term brain dysfunction in rats following cardiac arrest
topic rat model
ventricular fibrillation cardiac arrest
hippocampus
cortex
neurodegeneration
heme oxygenase
url https://www.mdpi.com/2218-273X/15/5/732
work_keys_str_mv AT wolfgangweihs neurologicdeficitscoreat45dayspostecprpredictslongtermbraindysfunctioninratsfollowingcardiacarrest
AT alexandramariastommel neurologicdeficitscoreat45dayspostecprpredictslongtermbraindysfunctioninratsfollowingcardiacarrest
AT andreamullebner neurologicdeficitscoreat45dayspostecprpredictslongtermbraindysfunctioninratsfollowingcardiacarrest
AT alexanderfranzszinovatz neurologicdeficitscoreat45dayspostecprpredictslongtermbraindysfunctioninratsfollowingcardiacarrest
AT matthiasmuller neurologicdeficitscoreat45dayspostecprpredictslongtermbraindysfunctioninratsfollowingcardiacarrest
AT ingridmagnet neurologicdeficitscoreat45dayspostecprpredictslongtermbraindysfunctioninratsfollowingcardiacarrest
AT michaelholzer neurologicdeficitscoreat45dayspostecprpredictslongtermbraindysfunctioninratsfollowingcardiacarrest
AT andreyvkozlov neurologicdeficitscoreat45dayspostecprpredictslongtermbraindysfunctioninratsfollowingcardiacarrest
AT sandrahogler neurologicdeficitscoreat45dayspostecprpredictslongtermbraindysfunctioninratsfollowingcardiacarrest
AT jcatharinaduvigneau neurologicdeficitscoreat45dayspostecprpredictslongtermbraindysfunctioninratsfollowingcardiacarrest