Cerebral hypoperfusion and delayed hippocampal response after induction of adult kaolin hydrocephalus.
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.
Klinge
Petra Margarete
PM
Department of Neurosurgery, Hannover Medical School, Hannover, Germany. pkllhydro@htp-tel.de
Samii
Amir
A
Mühlendyck
Annette
A
Visnyei
Koppany
K
Meyer
Geerd-Jürgen
GJ
Walter
Gerhard Franz
GF
Silverberg
Gerald D
GD
Brinker
Thomas
T
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
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