ArticleTranslational stroke research2023
Intracranial Pressure Dysfunction Following Severe Intracerebral Hemorrhage in Middle-Aged Rats.
Article in Translational stroke research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Incidence and characterization of spontaneous pituitary neuroendocrine tumors in aged spontaneously hypertensive rats.Scientific reports · 2025Article
- Evaluating the Monro-Kellie Doctrine: Contralateral Hemisphere Shrinkage in Intracerebral Hemorrhage Patients.Translational stroke research · 2025Article
- "Baihui" (DU20)-penetrating "Qubin" (GB7) acupuncture on blood-brain barrier integrity in rat intracerebral hemorrhage models via the RhoA/ROCK II/MLC 2 signaling pathway.Animal models and experimental medicine · 2024Article
- Tissue Compliance and Intracranial Pressure Responses to Large Intracerebral Hemorrhage in Young and Aged Spontaneously Hypertensive Rats.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Advances of nanotechnology for intracerebral hemorrhage therapy.Frontiers in bioengineering and biotechnology · 2023Review
- Relationship between edema and intracranial pressure following intracerebral hemorrhage in rat.Frontiers in stroke · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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
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