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(Stroke. 2003;34:193.)
© 2003 American Heart Association, Inc.

Original Contributions

Cerebral Hypoperfusion and Delayed Hippocampal Response After Induction of Adult Kaolin Hydrocephalus

Petra Margarete Klinge, MD; Amir Samii, MD; Annette Mühlendyck; Koppany Visnyei; Geerd-Jürgen Meyer, PhD; Gerhard Franz Walter, MD, PhD; Gerald D. Silverberg, MD Thomas Brinker, MD, PhD

From the Departments of Neurosurgery (P.M.K., A.M., K.V.), Nuclear Medicine (G-J.M.), and Neuropathology (G.F.W.), Hannover Medical School, Hannover, Germany; Department of Neurosurgery, Nordstadt Hospital Hannover (A.S., T.B.), Hannover, Germany; and Department of Neurosurgery, Stanford University Medical Center, Stanford, Calif (G.D.S.).

Correspondence to Petra Margarete Klinge, MD, Department of Neurosurgery, Hannover International Neuroscience Institute, D-30625 Hannover, Germany. E-mail pkllhydro{at}htp-tel.de

Background and Purpose— 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.

Key Words: autoradiography • cerebral ischemia • hippocampus • hydrocephalus • rats

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