Blocking VEGF by Bevacizumab Attenuates VEGF-Induced Vasospasm After Experimental Subarachnoid Hemorrhage in Rabbits

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dc.authoridGurer, Bora/0000-0003-1500-6184
dc.authoridBOZKURT, HUSEYIN/0000-0001-6432-5371
dc.authoridSahin, Omer Selcuk/0000-0003-2378-9537
dc.authoridTurkoglu, Erhan/0000-0001-7044-617X
dc.authorwosidGurer, Bora/K-1177-2012
dc.contributor.authorAkturk, Umut Dogu
dc.contributor.authorTuncer, Cengiz
dc.contributor.authorBozkurt, Huseyin
dc.contributor.authorSahin, Omer Selcuk
dc.contributor.authorBulut, Husamettin
dc.contributor.authorArikok, Ata
dc.contributor.authorTurkoglu, Erhan
dc.date.accessioned2021-12-01T18:51:03Z
dc.date.available2021-12-01T18:51:03Z
dc.date.issued2020
dc.department[Belirlenecek]en_US
dc.description.abstractOBJECTIVE: Vasospasm after subarachnoid hemorrhage (SAH) plays a vital role in the development of delayed cerebral ischemia. Anti-vascular endothelial growth factor (VEGF) antibodies, like bevacizumab (BEV), may attenuate VEGF-stimulated angiogenesis, reduced vascular cell proliferation, and improve vasospasm after SAH. METHODS: Thirty-two adult male New Zealand white rabbits were randomly divided into 4 groups of 8 rabbits in each group: group 1 (control); group 2 (SAH); group 3 (SAH + vehicle); and group 4 (SAH + BEV). BEV (5 mg/kg, intraperitoneally) was administered 5 minutes after the intracisternal blood injection and continued for 72 hours once per day in the same dose for group 4. Animals were sacrificed 72 hours after SAH. Basilar artery cross-sectional areas, arterial wall thicknesses, and hippocampal degeneration scores were evaluated in all groups. RESULTS: VEGF is associated with the narrowing of the basilar artery. Treatment with BEV statistically significantly increased the cross-sectional area of the basilar artery when compared with the SAH and the vehicle groups. Basilar artery wall thicknesses in the BEV group was statistically significant smaller than in the SAH and vehicle groups. The hippocampal degeneration scores for the BEV and control groups were similar and significantly lower than those for the SAH and vehicle groups. CONCLUSIONS: Cellular proliferation and subsequent vessel wall thickening is a reason to delay cerebral ischemia and deterioration of the neurocognitive function. Intraperitoneal administration of BEV was found to attenuate cerebral vasospasm and prevent delayed cerebral ischemia and improve neurocognitive function after SAH in rabbits.en_US
dc.identifier.doi10.1016/j.wneu.2020.03.151
dc.identifier.endpageE143en_US
dc.identifier.issn1878-8750
dc.identifier.issn1878-8769
dc.identifier.pmid32251821en_US
dc.identifier.scopus2-s2.0-85084201617en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpageE136en_US
dc.identifier.urihttps://doi.org/10.1016/j.wneu.2020.03.151
dc.identifier.urihttps://hdl.handle.net/20.500.12684/10961
dc.identifier.volume139en_US
dc.identifier.wosWOS:000550337100016en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherElsevier Science Incen_US
dc.relation.ispartofWorld Neurosurgeryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectBevacuzimaben_US
dc.subjectCerebral arteriesen_US
dc.subjectDelayed cerebral ischemiaen_US
dc.subjectHippocampusen_US
dc.subjectRabbiten_US
dc.subjectSubarachnoid hemorrhageen_US
dc.subjectVascular endothelial growth factoren_US
dc.subjectGrowth-Factor Vegfen_US
dc.subjectCerebral Vasospasmen_US
dc.subjectReceptor Antagonisten_US
dc.subjectAngiogenesisen_US
dc.subjectEfficacyen_US
dc.subjectTherapyen_US
dc.titleBlocking VEGF by Bevacizumab Attenuates VEGF-Induced Vasospasm After Experimental Subarachnoid Hemorrhage in Rabbitsen_US
dc.typeArticleen_US

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