title: Cerebral hypoperfusion and delayed hippocampal response after induction of adult kaolin hydrocephalus.
abstract: OBJECTIVE
  In chronic hydrocephalus, a role for tissue hypoxia resulting from cerebrovascular compression is suggested. The purpose of this study was to evaluate whether changes in cerebral blood flow (CBF) in the time course of adult kaolin-induced hydrocephalus correlated with immunohistochemical neuronal responses.
  
  
  METHODS
  In 46 adult Sprague-Dawley rats, kaolin hydrocephalus was induced and immunostaining of neurofilament protein (NF68), synaptophysin (SYN38), and neuronal nitric oxide synthase (NOS) was performed at 2 (short term), 4 (intermediate term), and 6 and 8 (long term) weeks. Local CBF was measured quantitatively by [14C]iodoantipyrine ([14C]IAP) autoradiography in the short-term stage and in both long-term stages.
  
  
  RESULTS
  At 2 weeks, neuronal NOS immunoreactivity was globally increased in cortical areas and within the hippocampus. Four weeks after hydrocephalus induction, a reactive increase of SYN38 and NF68 immunoreactivity in the periventricular cortex was seen. At 6 and 8 weeks, when the ventricular size was decreasing, immunohistochemical changes in the hippocampus became most evident. A maintained toxic NOS reactivity in the CA1 subfield was accompanied by a loss of NF68 staining. In the CA3 subfield, however, focal increases in NF68 and SYN38 immunoreactivity were found. Cortical and hippocampal blood flow showed prolonged decreases of 25% to 55% compared with control animals. At 8 weeks, control levels were reached.
  
  
  CONCLUSIONS
  The observed temporary CBF decrease appears to correlate with an early global neuronal ischemic response. In addition, it may also account for the delayed selective response of ischemia-vulnerable structures, eg, hippocampus, in chronic adult kaolin-induced hydrocephalus.
authors.affiliation: Department of Neurosurgery, Hannover Medical School, Hannover, Germany. pkllhydro@htp-tel.de
authors.forename: Petra Margarete
authors.initials: PM
authors.lastname: Klinge
authors.forename: Amir
authors.initials: A
authors.lastname: Samii
authors.forename: Annette
authors.initials: A
authors.lastname: Mühlendyck
authors.forename: Koppany
authors.initials: K
authors.lastname: Visnyei
authors.forename: Geerd-Jürgen
authors.initials: GJ
authors.lastname: Meyer
authors.forename: Gerhard Franz
authors.initials: GF
authors.lastname: Walter
authors.forename: Gerald D
authors.initials: GD
authors.lastname: Silverberg
authors.forename: Thomas
authors.initials: T
authors.lastname: Brinker
mesh_terms: D000818:Animals; D000983:Antipyrine / Q000031:analogs & derivatives*; D001345:Autoradiography; D002552:Cerebral Ventricles / Q000473:pathology; D002560:Cerebrovascular Circulation; D006624:Hippocampus / Q000098:blood supply / Q000201:enzymology / Q000378:metabolism*; D006849:Hydrocephalus / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology*; D007150:Immunohistochemistry; D007616:Kaolin; D007700:Kinetics; D008297:Male; D016900:Neurofilament Proteins / Q000276:immunology / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000276:immunology / Q000378:metabolism; D052248:Nitric Oxide Synthase Type I; D051381:Rats; D017207:Rats, Sprague-Dawley; D016708:Synaptophysin / Q000276:immunology / Q000378:metabolism
chemical_list: D016900:Neurofilament Proteins; D016708:Synaptophysin; C066858:neurofilament protein NF 68; D007616:Kaolin; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; C496322:Nos1 protein, rat; D000983:Antipyrine; C008135:iodoantipyrine