Long-term functional consequences and ongoing cerebral inflammation after subarachnoid hemorrhage in the rat.

Subarachnoid hemorrhage (SAH) represents a considerable health problem with an incidence of 6-7 per 100.000 individuals per year in Western society. We investigated the long-term consequences of SAH on behavior, neuroinflammation and gray- and white-matter damage using an endovascular puncture model...

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Autores principales:	Elke Kooijman, Cora H Nijboer, Cindy T J van Velthoven, Wouter Mol, Rick M Dijkhuizen, Jozef Kesecioglu, Cobi J Heijnen
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/e09f355636c143f6a8810e974396ad3f
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spelling	oai:doaj.org-article:e09f355636c143f6a8810e974396ad3f2021-11-18T08:29:27ZLong-term functional consequences and ongoing cerebral inflammation after subarachnoid hemorrhage in the rat.1932-620310.1371/journal.pone.0090584https://doaj.org/article/e09f355636c143f6a8810e974396ad3f2014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24603553/?tool=EBIhttps://doaj.org/toc/1932-6203Subarachnoid hemorrhage (SAH) represents a considerable health problem with an incidence of 6-7 per 100.000 individuals per year in Western society. We investigated the long-term consequences of SAH on behavior, neuroinflammation and gray- and white-matter damage using an endovascular puncture model in Wistar rats. Rats were divided into a mild or severe SAH group based on their acute neurological score at 24 h post-SAH. The degree of hemorrhage determined in post-mortem brains at 48 h strongly correlated with the acute neurological score. Severe SAH induced increased TNF-α, IL-1β, IL-10, MCP-1, MIP2, CINC-1 mRNA expression and cortical neutrophil influx at 48 h post-insult. Neuroinflammation after SAH was very long-lasting and still present at day 21 as determined by Iba-1 staining (microglia/macrophages) and GFAP (astrocytes). Long-term neuroinflammation was strongly associated with the degree of severity of SAH. Cerebral damage to gray- and white-matter was visualized by immunohistochemistry for MAP2 and MBP at 21 days after SAH. Severe SAH induced significant gray- and white-matter damage. MAP2 loss at day 21 correlated significantly with the acute neurological score determined at 24 h post-SAH. Sensorimotor behavior, determined by the adhesive removal task and von Frey test, was affected after severe SAH at day 21. In conclusion, we are the first to show that SAH induces ongoing cortical inflammation. Moreover, SAH induces mainly cortical long-term brain damage, which is associated with long-term sensorimotor damage.Elke KooijmanCora H NijboerCindy T J van VelthovenWouter MolRick M DijkhuizenJozef KeseciogluCobi J HeijnenPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 6, p e90584 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Elke Kooijman Cora H Nijboer Cindy T J van Velthoven Wouter Mol Rick M Dijkhuizen Jozef Kesecioglu Cobi J Heijnen Long-term functional consequences and ongoing cerebral inflammation after subarachnoid hemorrhage in the rat.
description	Subarachnoid hemorrhage (SAH) represents a considerable health problem with an incidence of 6-7 per 100.000 individuals per year in Western society. We investigated the long-term consequences of SAH on behavior, neuroinflammation and gray- and white-matter damage using an endovascular puncture model in Wistar rats. Rats were divided into a mild or severe SAH group based on their acute neurological score at 24 h post-SAH. The degree of hemorrhage determined in post-mortem brains at 48 h strongly correlated with the acute neurological score. Severe SAH induced increased TNF-α, IL-1β, IL-10, MCP-1, MIP2, CINC-1 mRNA expression and cortical neutrophil influx at 48 h post-insult. Neuroinflammation after SAH was very long-lasting and still present at day 21 as determined by Iba-1 staining (microglia/macrophages) and GFAP (astrocytes). Long-term neuroinflammation was strongly associated with the degree of severity of SAH. Cerebral damage to gray- and white-matter was visualized by immunohistochemistry for MAP2 and MBP at 21 days after SAH. Severe SAH induced significant gray- and white-matter damage. MAP2 loss at day 21 correlated significantly with the acute neurological score determined at 24 h post-SAH. Sensorimotor behavior, determined by the adhesive removal task and von Frey test, was affected after severe SAH at day 21. In conclusion, we are the first to show that SAH induces ongoing cortical inflammation. Moreover, SAH induces mainly cortical long-term brain damage, which is associated with long-term sensorimotor damage.
format	article
author	Elke Kooijman Cora H Nijboer Cindy T J van Velthoven Wouter Mol Rick M Dijkhuizen Jozef Kesecioglu Cobi J Heijnen
author_facet	Elke Kooijman Cora H Nijboer Cindy T J van Velthoven Wouter Mol Rick M Dijkhuizen Jozef Kesecioglu Cobi J Heijnen
author_sort	Elke Kooijman
title	Long-term functional consequences and ongoing cerebral inflammation after subarachnoid hemorrhage in the rat.
title_short	Long-term functional consequences and ongoing cerebral inflammation after subarachnoid hemorrhage in the rat.
title_full	Long-term functional consequences and ongoing cerebral inflammation after subarachnoid hemorrhage in the rat.
title_fullStr	Long-term functional consequences and ongoing cerebral inflammation after subarachnoid hemorrhage in the rat.
title_full_unstemmed	Long-term functional consequences and ongoing cerebral inflammation after subarachnoid hemorrhage in the rat.
title_sort	long-term functional consequences and ongoing cerebral inflammation after subarachnoid hemorrhage in the rat.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/e09f355636c143f6a8810e974396ad3f
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Long-term functional consequences and ongoing cerebral inflammation after subarachnoid hemorrhage in the rat.

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