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Intracranial Pressure Dysfunction Following Severe Intracerebral Hemorrhage in Middle-Aged Rats
Rising intracranial pressure (ICP) aggravates secondary injury and heightens risk of death following intracerebral hemorrhage (ICH). Long-recognized compensatory mechanisms that lower ICP include reduced cerebrospinal fluid and venous blood volumes. Recently, we identified another compensatory mecha...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer US
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10640482/ https://www.ncbi.nlm.nih.gov/pubmed/36367666 http://dx.doi.org/10.1007/s12975-022-01102-8 |
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author | Kalisvaart, Anna C. J. Abrahart, Ashley H. Coney, Alyvia T. Gu, Sherry Colbourne, Frederick |
author_facet | Kalisvaart, Anna C. J. Abrahart, Ashley H. Coney, Alyvia T. Gu, Sherry Colbourne, Frederick |
author_sort | Kalisvaart, Anna C. J. |
collection | PubMed |
description | Rising intracranial pressure (ICP) aggravates secondary injury and heightens risk of death following intracerebral hemorrhage (ICH). Long-recognized compensatory mechanisms that lower ICP include reduced cerebrospinal fluid and venous blood volumes. Recently, we identified another compensatory mechanism in severe stroke, a decrease in cerebral parenchymal volume via widespread reductions in cell volume and extracellular space (tissue compliance). Here, we examined how age affects tissue compliance and ICP dynamics after severe ICH in rats (collagenase model). A planned comparison to historical young animal data revealed that aged SHAMs (no stroke) had significant cerebral atrophy (9% reduction, p ≤ 0.05), ventricular enlargement (9% increase, p ≤ 0.05), and smaller CA1 neuron volumes (21%, p ≤ 0.05). After ICH in aged animals, contralateral striatal neuron density and CA1 astrocyte density significantly increased (12% for neurons, 7% for astrocytes, p ≤ 0.05 vs. aged SHAMs). Unlike young animals, other regions in aged animals did not display significantly reduced cell soma volume despite a few trends. Nonetheless, overall contralateral hemisphere volume was 10% smaller in aged ICH animals compared to aged SHAMs (p ≤ 0.05). This age-dependent pattern of tissue compliance is not due to absent ICH-associated mass effect (83.2 mm(3) avg. bleed volume) as aged ICH animals had significantly elevated mean and peak ICP (p ≤ 0.01), occurrence of ICP spiking events, as well as bilateral evidence of edema (e.g., 3% in injured brain, p ≤ 0.05 vs. aged SHAMs). Therefore, intracranial compliance reserve changes with age; after ICH, these and other age-related changes may cause greater fluctuation from baseline, increasing the chance of adverse outcomes like mortality. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12975-022-01102-8. |
format | Online Article Text |
id | pubmed-10640482 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-106404822023-11-14 Intracranial Pressure Dysfunction Following Severe Intracerebral Hemorrhage in Middle-Aged Rats Kalisvaart, Anna C. J. Abrahart, Ashley H. Coney, Alyvia T. Gu, Sherry Colbourne, Frederick Transl Stroke Res Research Rising intracranial pressure (ICP) aggravates secondary injury and heightens risk of death following intracerebral hemorrhage (ICH). Long-recognized compensatory mechanisms that lower ICP include reduced cerebrospinal fluid and venous blood volumes. Recently, we identified another compensatory mechanism in severe stroke, a decrease in cerebral parenchymal volume via widespread reductions in cell volume and extracellular space (tissue compliance). Here, we examined how age affects tissue compliance and ICP dynamics after severe ICH in rats (collagenase model). A planned comparison to historical young animal data revealed that aged SHAMs (no stroke) had significant cerebral atrophy (9% reduction, p ≤ 0.05), ventricular enlargement (9% increase, p ≤ 0.05), and smaller CA1 neuron volumes (21%, p ≤ 0.05). After ICH in aged animals, contralateral striatal neuron density and CA1 astrocyte density significantly increased (12% for neurons, 7% for astrocytes, p ≤ 0.05 vs. aged SHAMs). Unlike young animals, other regions in aged animals did not display significantly reduced cell soma volume despite a few trends. Nonetheless, overall contralateral hemisphere volume was 10% smaller in aged ICH animals compared to aged SHAMs (p ≤ 0.05). This age-dependent pattern of tissue compliance is not due to absent ICH-associated mass effect (83.2 mm(3) avg. bleed volume) as aged ICH animals had significantly elevated mean and peak ICP (p ≤ 0.01), occurrence of ICP spiking events, as well as bilateral evidence of edema (e.g., 3% in injured brain, p ≤ 0.05 vs. aged SHAMs). Therefore, intracranial compliance reserve changes with age; after ICH, these and other age-related changes may cause greater fluctuation from baseline, increasing the chance of adverse outcomes like mortality. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12975-022-01102-8. Springer US 2022-11-11 2023 /pmc/articles/PMC10640482/ /pubmed/36367666 http://dx.doi.org/10.1007/s12975-022-01102-8 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Research Kalisvaart, Anna C. J. Abrahart, Ashley H. Coney, Alyvia T. Gu, Sherry Colbourne, Frederick Intracranial Pressure Dysfunction Following Severe Intracerebral Hemorrhage in Middle-Aged Rats |
title | Intracranial Pressure Dysfunction Following Severe Intracerebral Hemorrhage in Middle-Aged Rats |
title_full | Intracranial Pressure Dysfunction Following Severe Intracerebral Hemorrhage in Middle-Aged Rats |
title_fullStr | Intracranial Pressure Dysfunction Following Severe Intracerebral Hemorrhage in Middle-Aged Rats |
title_full_unstemmed | Intracranial Pressure Dysfunction Following Severe Intracerebral Hemorrhage in Middle-Aged Rats |
title_short | Intracranial Pressure Dysfunction Following Severe Intracerebral Hemorrhage in Middle-Aged Rats |
title_sort | intracranial pressure dysfunction following severe intracerebral hemorrhage in middle-aged rats |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10640482/ https://www.ncbi.nlm.nih.gov/pubmed/36367666 http://dx.doi.org/10.1007/s12975-022-01102-8 |
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