gms | German Medical Science

57th Annual Meeting of the German Society of Neurosurgery
Joint Meeting with the Japanese Neurosurgical Society

German Society of Neurosurgery (DGNC)

11 - 14 May, Essen

Endothelial progenitor cells (EPCs) restore chronically impaired cerebral hemodynamics in rats

Endotheliale Vorläuferzellen (EPCs) verbessern chronische zerebrale hämodynamische Einschränkung im Rattenmodell

Meeting Abstract

  • corresponding author U.C. Schneider - Neurochirurgische Klinik, Universitätsklinikum Mannheim
  • N. Hecht - Neurochirurgische Klinik, Universitätsklinikum Mannheim
  • J. Woitzik - Neurochirurgische Klinik, Universitätsklinikum Mannheim
  • P. Vajkoczy - Neurochirurgische Klinik, Universitätsklinikum Mannheim

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 57. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie. Essen, 11.-14.05.2006. Düsseldorf, Köln: German Medical Science; 2006. DocP 06.88

The electronic version of this article is the complete one and can be found online at:

Published: May 8, 2006

© 2006 Schneider et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Objective: Endothelial progenitor cells (EPCs) have been reported to have significant therapeutic potential after hypoxic or ischemic injury by enhancing neovascularisation. Aim of this study was to determine the effect of systemically administered mouse embryonal EPCs on cerebral hemodynamics and on the vasculature in a rat model of chronic mild impairment of the cerebral perfusion.

Methods: 30 male Sprague-Dawley rats were randomly assigned to one of the following treatment groups: (i) bilateral occlusion of the vertebral arteries, occlusion of the right common carotid artery (3-VO) and EPC treatment (1million cells in 1ml medium administered weekly via the tail vein; EPC group), (ii) 3-VO and vehicle treatment (control group) and (iii) sham-occlusion and vehicle treatment (sham group). Cerebral reserve capacity (CVRC) was assessed by laser-Doppler flowmetry (LDF) (acetazolamide stimulation). After three weeks, neovascularisation was assessed by intra-arterial latex or Evans Blue infusion. Capillaries were counted and the diameter of large conductance arteries was measured.

Results: One week after 3-VO, a loss of the acetazolamide-induced LDF increase was observed in control animals, while in sham and EPC animals CVRC values remained at baseline levels (EPC 13.7±6.2; Control 1.5± 2.2%; Sham 7.3±6.4%). The number of capillaries per observation field was significantly higher in EPC animals than in control and sham animals (EPC 81±14; Control 72±8; Sham 67±5). There was no change in diameter of the large conductance arteries.

Conclusions: A model of 3-VO in rats leads to a significant impairment of CVRC indicating severe blood flow regulation deficits. Treatment with EPCs normalizes these deficits and may therefore serve as new therapy for hemodynamic cerebrovascular insufficiency.