London, United Kingdom 2013 Poster Session Red Cerebrovasc Dis 2013; 35 (suppl 3)1-854 537 470 Experimental studies Characterization of cerebral small vessel disease in SHRSP: A longitudinal MRI study at 3.0 Tesla S. Mencl1, H. Braun2, C. Garz3, C Bueche4, E. Goeb5, G. Homola6, H-J. Heinze7, M. Goertler8, K.G. Reymann9, C. Kleinschnitz10, S. Schreiber11 Department of Neurology, University Hospital of Wuerzburg, Wuerzburg, GERMANY1, German Center for Neurodegenerative Diseases, Magdeburg, GERMANY2, Department of Neu-rology, Otto-von-Guericke-University, Magdeburg, GERMANY3, Department of Neurology, Ot-to- von-Guericke-University, Magdeburg, GERMANY4, Department of Neurology, University Hos-pital of Wuerzburg, Wuerzburg, GERMANY5, Department of Neuroradiology, University Hospital of Wuerzburg, Wuerzburg, GERMANY6, Department of Neurology, Otto-von-Guericke-University, Magdeburg, GERMANY7, Department of Neurology, Otto-von-Guericke-University, Magdeburg, GERMANY8, German Center for Neurodegenerative Diseases, Leibniz Institute for Neurobiology,, Magdeburg, GERMANY9,Department of Neurology, University Hospital of Wuerzburg, Wuerzburg, GERMANY10, Department of Neurology, Otto-von-Guericke-University, Wuerzburg, GERMANY11 Background: Human cerebral small vessel disease (CSVD, cerebral microangiopathy) is one of the leading causes of vascular dementia and ischemic stroke and is caused by degenerative small vessel wall chang-es. In spontaneously hypertensive stroke-prone rats (SHRSP), a well-established animal model of CSVD, we recently showed that cerebral microangiopathy develops in distinct histopathological steps initiated by intracapillary and –arteriolar erythrocyte accumulations. This early microvascular dysfunction is followed by blood brain barrier (BBB) disruption, subsequent microbleeds and final-ly hemorrhagic infarcts and intraparenchymal hermorrhage. In the present study we aimed to verify this pathophysiological cascade non-invasively by serial magnetic resonance imaging (MRI). Methods: Fourteen SHRSP and three control rats (Wistar) aged between 26 and 42 weeks were repeatedly investigated by 3.0 Tesla MRI (Siemens Trio) including T1-weighted, T2-weighted, T2 CISS 3D, FLAIR and GRE images. Animals were perfused for H&E staining at (i) an age of 42 weeks or (ii) after developing stroke-like symptoms or (iii) as soon as MRI revealed pathologies including hyper- or hypointensities. Histology was correlated with the MRI data Results: Terminal stages of the CSVD cascade, including larger intraparenchymal hemorrhages and infarcts could be consistently detected by MRI and were confirmed histologically. However, 3.0 Tesla MRI failed to visualize microbleeds (< 150 mm) which were frequently found in histology. Moreover, there was no MRI correlate of the initial microvascular dysfunction including luminal erythrocyte accumulations in small brain vessels. Conclusion: MRI at field strength of 3.0 Tesla can only partially depict the pathological changes in the brains of SHRSP. Further investigations at higher magnetic field strengths (7.0 Tesla) using blood- and flow-sensitive sequences are currently underway to increase the diagnostic sensitivity. 471 Experimental studies COMPARATION BETWEEN XENOGENIC AND ALLOGENIC ADIPOSSE TISSUE MES-ENCHYMAL STEM CELLS IN TREATMENT OF ACUTE CEREBRAL INFARCT. CON-CEPT PROOF IN RATS M. Gutiérrez-Fernández1, B. Rodríguez-Frutos2, J. Ramos-Cejudo3, B. Fuentes4, E. Díez-Tejedor5 Neurology Department, Neuroscience and Cerebrovascular Research Laboratory. La Paz University Hospital, IdiPAZ, UAM, Madrid, SPAIN1, Neurology Department, Neuroscience and Cerebrovascular Research Laboratory. La Paz University Hospital, IdiPAZ, UAM, Madrid, SPAIN2, Neurology Department, Neuroscience and Cerebrovascular Research Laboratory. La Paz University Hospital, IdiPAZ, UAM, Madrid, SPAIN3, Neurology Department, Neuroscience and Cerebrovas-cular Research Laboratory. La Paz University Hospital, IdiPAZ, UAM, Madrid, SPAIN4, Neurology Department, Neuroscience and Cerebrovascular Research Laboratory. La Paz University Hospital, IdiPAZ, UAM, Madrid, SPAIN5 Background: It has been suggested that mesenchymal stem cells (MSC) are appropriate for stroke treatment, demonstrating safety, feasibility and efficacy. However, more information regarding ap-propriate cell type is needed from animal model. Therefore, it would be interesting to perform a con-cept proof: to administer the human Adipose Tissue-derived-MSC (hAD-MSC) (xenogenic admin-istration) to demonstrate the safety itself in the animal model. Aims: To study the safety and the of acute intravenous (i.v.) xenogenic administration of hAD-MSC or allogenic rat Adipose Tissue-de-rived- MSC (rAD-MSC) on functional evaluation in rat model of permanent Middle Cerebral Artery Occlusion (pMCAO).Methods: Model of pMCAO in male rats in 4 groups (n=10): a) Sham; b) Con-trol: surgery + infarct; c) hAD-MSC: surgery+infarct+i.v hAD-MSC (2X106 cells); d) rAD-MSC:- surgery+infarct+i.v rAD-MSC (2X106 cells). We analyzed: functional evaluation by the Rogers test; infarct volume by Magnetic Resonance Imaging (MRI) and Hematoxilin-Eosin (H-E); cell migra-tion and implantation by MRI and inmmunohistochemistry. All theses parameters were analyzed at 24h and 14 days. Cell death by TUNEL at 14 days and tumor formation at 3 months. Results: Compared to Control group,a significant improvement in recovery was found at 24h and continued at 14d after i.v. administration of either hAD-MSC or rAD-MSC (p<0,05).No reduction in infarct volume or any migration/implantation of cells into the damaged brain were observed in the treatment groups. Nevertheless,cell death was reduced significantly in both treatment groups with respect to the Control group (p<0,05).We did not observe tumor formation at 3 months in none treat-ment groups. Conclusion: The administration of hAD-MSC or rAD-MSC demonstrated equal efficacy on func-tional recovery and decreased ischemic brain damage (reduction cell death). Besides, both treatment groups have demonstrated safety without side effects nor tumor formation.
Karger_ESC London_2013
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