Tibo Gerriets , Erwin Stolz , Maureen Walberer , Clemens Müller , Alexander Kluge , Manfred Kaps , Marc Fisher , Georg Bachmann
{"title":"Middle cerebral artery occlusion during MR-imaging: investigation of the hyperacute phase of stroke using a new in-bore occlusion model in rats","authors":"Tibo Gerriets , Erwin Stolz , Maureen Walberer , Clemens Müller , Alexander Kluge , Manfred Kaps , Marc Fisher , Georg Bachmann","doi":"10.1016/j.brainresprot.2003.08.006","DOIUrl":null,"url":null,"abstract":"<div><p>Magnetic resonance imaging (MRI) provides insights into the dynamics of focal cerebral ischemia. Usually, experimental stroke is induced outside the magnet bore, preventing investigators from acquiring pre-ischemic images for later pixel-by-pixel comparisons and from studying the earliest changes in the hyperacute phase of ischemia. Herein, we introduce a new and easy to apply in-bore occlusion protocol based on the intraarterial embolization of ceramic macrospheres.</p><p><span>PE-50 tubing, filled with saline and six macrospheres (0.315–0.355 mm in diameter), was placed into the internal carotid artery (ICA) of anesthetized Sprague–Dawley rats. The animals were transferred into an MRI scanner (7.0 T) and baseline diffusion-weighted imaging (DWI) and T2-imaging was performed. Then the macrospheres were injected into the internal artery to occlude the </span>MCA. Post-ischemic DWI and T2-imaging was started immediately thereafter. The apparent diffusion coefficient (ADC) (a marker for cytotoxic brain edema) and T2-relaxation time (a marker for vasogenic brain edema) were determined in the ischemic lesions and compared to the unaffected hemisphere.</p><p>ADC significantly declined within the first 5–10 min after stroke onset. T2-relaxation time increased as early as at the first T2-imaging time-point (20–35 min after embolization). After 150 min of ischemia, the lesions covered 18.0±7.4% of the hemispheres. The model failed in one out of nine animals (11%).</p><p>This model allows MR-imaging from the initial minutes after permanent middle cerebral artery (MCA) occlusion. It does not permit reperfusion. This technique might provide information about the pathophysiological processes in the hyperacute phase of stroke.</p></div>","PeriodicalId":79477,"journal":{"name":"Brain research. Brain research protocols","volume":"12 3","pages":"Pages 137-143"},"PeriodicalIF":0.0000,"publicationDate":"2004-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.brainresprot.2003.08.006","citationCount":"54","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Brain research. Brain research protocols","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1385299X03001089","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 54
Abstract
Magnetic resonance imaging (MRI) provides insights into the dynamics of focal cerebral ischemia. Usually, experimental stroke is induced outside the magnet bore, preventing investigators from acquiring pre-ischemic images for later pixel-by-pixel comparisons and from studying the earliest changes in the hyperacute phase of ischemia. Herein, we introduce a new and easy to apply in-bore occlusion protocol based on the intraarterial embolization of ceramic macrospheres.
PE-50 tubing, filled with saline and six macrospheres (0.315–0.355 mm in diameter), was placed into the internal carotid artery (ICA) of anesthetized Sprague–Dawley rats. The animals were transferred into an MRI scanner (7.0 T) and baseline diffusion-weighted imaging (DWI) and T2-imaging was performed. Then the macrospheres were injected into the internal artery to occlude the MCA. Post-ischemic DWI and T2-imaging was started immediately thereafter. The apparent diffusion coefficient (ADC) (a marker for cytotoxic brain edema) and T2-relaxation time (a marker for vasogenic brain edema) were determined in the ischemic lesions and compared to the unaffected hemisphere.
ADC significantly declined within the first 5–10 min after stroke onset. T2-relaxation time increased as early as at the first T2-imaging time-point (20–35 min after embolization). After 150 min of ischemia, the lesions covered 18.0±7.4% of the hemispheres. The model failed in one out of nine animals (11%).
This model allows MR-imaging from the initial minutes after permanent middle cerebral artery (MCA) occlusion. It does not permit reperfusion. This technique might provide information about the pathophysiological processes in the hyperacute phase of stroke.