gms | German Medical Science

63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

13. - 16. Juni 2012, Leipzig

A new rodent model of caudate lacunar infarction – Ultrastructure, histology, brain edema and behavior change

Meeting Abstract

Suche in Medline nach

  • T. Kuroiwa - Laboratory of Clinical Medicine, Namegata District General Hospital, Ibaraki Japan
  • H. Tabata - Department of Neurosurgery, Namegata District General Hospital, Ibaraki Japan
  • G. Xi - Department of Neurosurgery, University of Michigan, Ann Arbor, United States
  • R.F. Keep - Department of Neurosurgery, University of Michigan, Ann Arbor, United States

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS). Leipzig, 13.-16.06.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. DocP 023

DOI: 10.3205/12dgnc410, URN: urn:nbn:de:0183-12dgnc4105

Veröffentlicht: 4. Juni 2012

© 2012 Kuroiwa et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: Although there are numerous animal models of cerebral ischemia induced by large intracranial artery occlusion, no entirely satisfactory model of lacunar infarction is available. We have developed a rodent model of lacunar infarction induced by photothrombotic occlusion of the small vessels within the caudate nucleus and subsequently characterized.

Methods: Male SD rats (n=63) and Mongolian gerbils (n=8) were anesthetized, and Rose Bengal dye was intravenously injected. The left caudate nucleus was exposed to cold white light for 5 to 10 minutes via a stereotaxically implanted polymethylmethacrylate optic fiber (0.5 mm diameter). Neurological and morphological changes as well as brain edema were assessed at various times during the following 6 weeks (n=50). Regional cerebral blood flow was quantified by 14C-IMP autoradiography at 1.5 h after photothrobosis (n=11), ultrastructural changes of the small parenchymal vessels and neuropile were examined at 4 h after photothrombosis (n=2).

Results: A round infarction surrounded by a layer of selective neuronal death was formed in the caudate nucleus around the tip of optic fiber, which turned into a lacune (cystic cavity) over 6 weeks post-lesioning. rCBF map revealed a central zone of markedly reduced blood flow with surrounding oligemic zone. Early blood-brain barrier opening with edema peaked at day 1. Increased pinocytotic vesicles in the small vessels and platelet thrombus formation were observed in the lesion. Neurological deficits including foot fault placing in rats and impaired beam walking in gerbils was observed after photothrombosis, and the severity and duration of neurological deficits paralleled the infarct size.

Conclusions: We have developed a rodent model of lacunar infarction by photothrombotic occlusion of the microvessels within the caudate nucleus. The initial edematous lesion turned into lacune over 6 weeks of post ischemia. The current caudate photothrombosis model of lacunar infarction appears suitable for future therapeutic and behavioral studies on lacunar infarction.