TRADITIONAL POSTER - ismrm
TRADITIONAL POSTER - ismrm
TRADITIONAL POSTER - ismrm
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Poster Sessions<br />
2237. tPA-Induced Suppression of Cerebrovascular Parameters in Acute Rat Stroke Model: Dynamic MRI<br />
Study<br />
Young Ro Kim 1 , Xiang Fan 2 , Guangping Dai 1 , Jeong Kon Kim 3 , Bruce R. Rosen 1 , xiaoying Wang 2<br />
1 Radiology, Martinos Center for Biomedical Imaging / Massachusetts General Hospital, Charlestown, MA, United States; 2 Radiology,<br />
Neuroprotection Research laboratory / Massachusetts General Hospital, Charlestown, MA, United States; 3 Radiology, Asan Medical<br />
Center, Seoul, Korea, Republic of<br />
Tissue plasminogen activator (tPA) has been frequently used for treating acute ischemic stroke based on re-canalization, reopening of occluded vessels for<br />
the reinstitution of regional blood perfusion. Despite the promising clinical outcomes, exogenous tPA may worsen the ischemia-induced blood brain-barrier<br />
disruption, elevate risks of intracranial hemorrhage, and in part consequently reduces the therapeutic time window. Therefore, it is critically important to<br />
understand the overall effects of tPA treatment on cerebrohemodynamics. In this study, we investigated the vasoreactivity in response to intravenously<br />
administered tPA and to systemic hypercapnia before and after tPA using a permanent focal stroke rat model.<br />
2238. Validation of T2* Weight Signal Change of Oxygen Challenge as a Potential Better Penumbra<br />
Estimation<br />
Fang Du 1 , Shiliang Huang 1 , Qiang Shen 1 , Timothy Q. Duong 1<br />
1 Research Imaging Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX, United States<br />
Mismatch of diffusion/perfusion by MRI has been used as an estimate of the ischemic penumbra, but there are large parts of the mismatch region appear not<br />
to at risk and it was also reported that some of the apparent diffusion coefficient reduction area can be salvaged by early reperfusion. It was proposed that<br />
T2* weight signal change of oxygen challenge could be a better penumbra estimation. This study applied OC technique to a group of transient ischemia rats<br />
and proved this hypothesis.<br />
2239. MRI of Emboli Localization and Lysis in an Embolic Model of Rat Middle Cerebral Artery Occlusion<br />
Ronn Philip Walvick 1 , Bernt Torre Bratane 2 , James Bouley 2 , Nills Henninger 2 , Mitchell Albert 1 , Marc<br />
Fisher 1<br />
1 Radiology, University of Massachusetts Medical School, Worcester, MA, United States; 2 Neurology, University of Massachusetts<br />
Medical School, Worcester, MA, United States<br />
We present a novel technique to localize and observe the dynamics of clot lysis during tissue Plasminogen Activator (tPA). Prior to fabrication of clots,<br />
blood was doped with Magnevist (Bayer, Wayne, NJ). Clots were withdrawn tubing and injected into the left common carotid artery at the base of the skull<br />
causing a middle cerebral artery occlusion. MRI consisted of diffusion, perfusion, and T1 weighted imaging for clot localization, and MR angiography.<br />
During tPA administration, serial T1 weighted and perfusion imaging was performed. Our results demonstrate the ability of this method to detect clots in a<br />
preclinical model of embolic stroke.<br />
2240. Magnetic Resonance Imaging as an In-Vivo Tool for Evaluating Efficacy of Brain Edema Prevention<br />
Therapy in a Rat Stroke Model<br />
Denise C. Welsh 1 , Andrew Danziger 2 , Theodore Detwiler 2 , Hillary Regan 2 , Joseph J. Lynch 2 , Christopher<br />
P. Regan 2 , Donald S. Williams 1 , Alexandre Coimbra 1<br />
1 Imaging, Merck, West Point, Pa, United States; 2 Central Pharmacology, Merck, West Point, Pa, United States<br />
While numerous studies have used MRI techniques for studying stroke pathology, there has been limited use of MR parameters as in vivo markers of novel<br />
treatment efficacy. Here, Gd-enhanced T1-w and T2-w MR data were used to verify the efficacy of pre- and post-infarct treatment with a novel KDR kinase<br />
inhibitor (KDRi) known to reduce vascular permeability and therefore, BBB leakage. In line with previously published ex-vivo data (1), in-vivo MRI results<br />
suggest efficacy of KDRi treatment in reducing BBB leakage and edema formation, as indicated by tissue water content.<br />
2241. Longitudinal Assessment of Brain Damage in Hypertension Rats Using Diffusion Tensor Imaging<br />
Chien-Yuan Lin 1 , Cheng-Di Chiu 2,3 , Ming-Huang Lin 1 , Wai-Mui Cheung 1 , Teng-Nan Lin 1 , Chen Chang 1<br />
1 Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan; 2 Graduate Institute of Medical Sciences, National Defense<br />
Medical Center, Taipei, Taiwan; 3 Department of Neurosurgery, Chang-Hua Hospital, Chang-Hua, Taiwan<br />
The elevated blood pressure is considered to be the main risk factor of stroke and is highly associated with white matter lesions. This study aimed to<br />
investigate the change of white matter microstructure under various levels of blood pressures.<br />
2242. MRI Monitoring of Endogenous Stem Cell Therapies in Animal Models of Stroke<br />
Voytek Gretka 1 , Lisa Di Diodato 1 , Amy Hoyles 2 , Nancy J. Lobaugh 3 , Cindi Morshead 2 , Greg J. Stanisz 1<br />
1 Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada; 2 Department of Surgery, University of Toronto,<br />
Toronto, ON, Canada; 3 Cognitive Neurology, Sunnybrook Health Sciences Centre, Toronto, ON, Canada<br />
In animal models of stroke, endogenous neural precursor cells can be activated with growth factors such as epidermal growth factor (EGF) and<br />
erythropoietin (EPO) leading to increased neurogenesis and behavioural recovery. We demonstrated the feasibility of using MR to distinguish between<br />
regenerating and pathological tissues when using endogenous stem cell therapies in rats. Tissue growth in the lesion site has MR characteristics (T 1 and T 2 )<br />
similar to that of normal brain tissue, and differs distinctly from the cavity present when animals are untreated. MRI is able to predict the outcome of the<br />
treatment as early as 2 weeks post stroke.