title: Dissociation between vascular endothelial growth factor receptor-2 and blood vessel density in the caudate nucleus after chronic hydrocephalus.
abstract: Chronic hydrocephalus (CH) is characterized by the presence of ventricular enlargement, decreased cerebral blood flow (CBF), and brain tissue oxygen delivery. Although the underlying pathophysiological role of vascular endothelial growth factor (VEGF) is not clear, ischemic-hypoxic events in CH are known to trigger its release. Previously, we have shown increased VEGF receptor-2 (VEGFR-2) and blood vessel density (BVd) in the hippocampus after CH. We investigated changes in neuronal and glial VEGFR-2 density and BVd in the caudate nucleus in an experimental model of CH. Animals with CH were divided into short term (ST, 2 to 4 weeks) and long term (LT, 12 to 16 weeks) and were compared with surgical controls (SCs, 12 to 16 weeks). The cellular and BVds were estimated using immunohistochemical and stereological counting methods. Overall, percentage (%)VEGFR-2 neurons were approximately two times greater in CH (ST, LT) than in SC. By comparison, glial cell %VEGFR-2 was greater by 10% to 17% in ST and 4% to 11% lower in LT compared with that in SC. Blood vessel density was significantly lower in CH than in SC in the superficial caudate. Changes in cerebrospinal fluid ventricular volume and pressure, as well as in CBF did not correlate with either VEGFR-2 or BVd. These observed findings suggest that destructive forces may outweigh angiogenic forces and possibly show a disassociation between VEGFR-2 and BV expressions.
authors.affiliation: Department of Neurological Surgery, Section of Pediatric and Congenital Neurological Surgery, CSF Physiology Laboratory, Neurological Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA.
authors.forename: Abhishek
authors.initials: A
authors.lastname: Deshpande
authors.forename: Stephen M
authors.initials: SM
authors.lastname: Dombrowski
authors.forename: Anna
authors.initials: A
authors.lastname: Leichliter
authors.forename: Natalie
authors.initials: N
authors.lastname: Krajcir
authors.forename: Nicholas
authors.initials: N
authors.lastname: Zingales
authors.forename: Masahiro
authors.initials: M
authors.lastname: Inoue
authors.forename: Soren
authors.initials: S
authors.lastname: Schenk
authors.forename: Kiyotaka
authors.initials: K
authors.lastname: Fukamachi
authors.forename: Mark G
authors.initials: MG
authors.lastname: Luciano
mesh_terms: D000818:Animals; D002302:Cardiac Output / Q000502:physiology; D002421:Caudate Nucleus / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D002452:Cell Count; D002560:Cerebrovascular Circulation / Q000502:physiology; D002908:Chronic Disease; D004195:Disease Models, Animal; D004285:Dogs; D006849:Hydrocephalus / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D007150:Immunohistochemistry; D007427:Intracranial Pressure / Q000502:physiology; D008279:Magnetic Resonance Imaging; D008297:Male; D018919:Neovascularization, Physiologic; D009457:Neuroglia / Q000378:metabolism / Q000473:pathology; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000378:metabolism*
chemical_list: D040301:Vascular Endothelial Growth Factor Receptor-2