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dc.contributor.authorBardutzky, Juergen F.
dc.contributor.authorMeng, Xiangjun
dc.contributor.authorBouley, James P.
dc.contributor.authorDuong, Timothy Q.
dc.contributor.authorRatan, Rajiv
dc.contributor.authorFisher, Marc
dc.date2022-08-11T08:09:27.000
dc.date.accessioned2022-08-23T16:31:23Z
dc.date.available2022-08-23T16:31:23Z
dc.date.issued2005-03-04
dc.date.submitted2008-04-28
dc.identifier.citationJ Cereb Blood Flow Metab. 2005 Aug;25(8):968-77. <a href="http://dx.doi.org/10.1038/sj.jcbfm.9600095">Link to article on publisher's site</a>
dc.identifier.issn0271-678X (Print)
dc.identifier.doi10.1038/sj.jcbfm.9600095
dc.identifier.pmid15744247
dc.identifier.urihttp://hdl.handle.net/20.500.14038/37631
dc.description.abstractDimethyl sulfoxide (DMSO) has a variety of biological actions that suggest efficacy as a neuroprotectant. We (1) tested the neuroprotective potential of DMSO at different time windows on infarct size using 2,3,5-triphenyltetrazolium staining and (2) investigated the effects of DMSO on ischemia evolution using quantitative diffusion and perfusion imaging in a permanent middle cerebral artery occlusion (MCAO) model in rats. In experiment 1, DMSO treatment (1.5 g/kg intravenously over 3 h) reduced infarct volume 24 h after MCAO by 65% (P<0.00001) when initiated 20 h before MCAO, by 44% (P=0.0006) when initiated 1 h after MCAO, and by 17% (P=0.11) when started 2 h after MCAO. Significant infarct reduction was also observed after a 3-day survival in animals treated 1 h after MCAO (P=0.005). In experiment 2, treatment was initiated 1 h after MCAO and maps for cerebral blood flow (CBF) and apparent diffusion coefficient (ADC) were acquired before treatment and then every 30 mins up to 4 h. Cerebral blood flow characteristics and CBF-derived lesion volumes did not differ between treated and untreated animals, whereas the ADC-derived lesion volume essentially stopped progressing during DMSO treatment, resulting in a persistent diffusion/perfusion mismatch. This effect was mainly observed in the cortex. Our data suggest that DMSO represents an interesting candidate for acute stroke treatment.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15744247&dopt=Abstract ">Link to article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1038/sj.jcbfm.9600095
dc.subjectAnimals
dc.subjectBehavior, Animal
dc.subjectBlood Pressure
dc.subjectBody Temperature
dc.subjectBrain
dc.subjectBrain Ischemia
dc.subjectCerebrovascular Circulation
dc.subjectDiffusion Magnetic Resonance Imaging
dc.subjectDimethyl Sulfoxide
dc.subjectDisease Progression
dc.subjectFunctional Laterality
dc.subjectHeart Rate
dc.subjectInfarction, Middle Cerebral Artery
dc.subjectInjections, Intravenous
dc.subjectMale
dc.subject*Neuroprotective Agents
dc.subjectRats
dc.subjectRats, Inbred WKY
dc.subjectNervous System Diseases
dc.subjectNeurology
dc.titleEffects of intravenous dimethyl sulfoxide on ischemia evolution in a rat permanent occlusion model
dc.typeJournal Article
dc.source.journaltitleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
dc.source.volume25
dc.source.issue8
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/neuro_pp/174
dc.identifier.contextkey499356
html.description.abstract<p>Dimethyl sulfoxide (DMSO) has a variety of biological actions that suggest efficacy as a neuroprotectant. We (1) tested the neuroprotective potential of DMSO at different time windows on infarct size using 2,3,5-triphenyltetrazolium staining and (2) investigated the effects of DMSO on ischemia evolution using quantitative diffusion and perfusion imaging in a permanent middle cerebral artery occlusion (MCAO) model in rats. In experiment 1, DMSO treatment (1.5 g/kg intravenously over 3 h) reduced infarct volume 24 h after MCAO by 65% (P<0.00001) when initiated 20 h before MCAO, by 44% (P=0.0006) when initiated 1 h after MCAO, and by 17% (P=0.11) when started 2 h after MCAO. Significant infarct reduction was also observed after a 3-day survival in animals treated 1 h after MCAO (P=0.005). In experiment 2, treatment was initiated 1 h after MCAO and maps for cerebral blood flow (CBF) and apparent diffusion coefficient (ADC) were acquired before treatment and then every 30 mins up to 4 h. Cerebral blood flow characteristics and CBF-derived lesion volumes did not differ between treated and untreated animals, whereas the ADC-derived lesion volume essentially stopped progressing during DMSO treatment, resulting in a persistent diffusion/perfusion mismatch. This effect was mainly observed in the cortex. Our data suggest that DMSO represents an interesting candidate for acute stroke treatment.</p>
dc.identifier.submissionpathneuro_pp/174
dc.contributor.departmentDepartment of Neurology
dc.source.pages968-77


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