Delayed treatment with intravenous basic fibroblast growth factor reduces infarct size following permanent focal cerebral ischemia in rats

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dc.contributor.authorFisher, Marc
dc.contributor.authorMeadows, Mary-Ellen
dc.contributor.authorDo, Tuyen
dc.contributor.authorWeise, Jens
dc.contributor.authorTrubetskoy, Vladimir
dc.contributor.authorCharette, Marc
dc.contributor.authorFinklestein, Seth P.
dc.contributor.departmentDepartment of Neurology
dc.date2022-08-11T08:09:26.000
dc.date.accessioned2022-08-23T16:31:05Z
dc.date.available2022-08-23T16:31:05Z
dc.date.issued1995-11-01
dc.date.submitted2008-04-17
dc.description.abstractBasic fibroblast growth factor (bFGF) is a polypeptide that supports the survival of brain cells (including neurons, glia, and endothelia) and protects neurons against a number of toxins and insults in vitro. This factor is also a potent dilator of cerebral pial arterioles in vivo. In previous studies, we found that intraventricularly administered bFGF reduced infarct volume in a model of focal cerebral ischemia in rats. In the current study, bFGF (45 micrograms/kg/h) in vehicle, or vehicle alone, was infused intravenously for 3 h, beginning at 30 min after permanent middle cerebral artery occlusion by intraluminal suture in mature Sprague-Dawley rats. After 24 h, neurological deficit (as assessed by a 0- to 5-point scale, with 5 = most severe) was 2.6 +/- 1.0 in vehicle-treated and 1.5 +/- 1.3 in bFGF-treated rats (mean +/- SD; N = 12 vs. 11; p = 0.009). Infarct volume was 297 +/- 65 mm3 in vehicle- and 143 +/- 135 mm3 in bFGF-treated animals (p = 0.002). During infusion, there was a modest decrease in mean arterial blood pressure but no changes in arterial blood gases or core or brain temperature in bFGF-treated rats. Autoradiography following intravenous administration of 111In-labeled bFGF showed that labeled bFGF crossed the damaged blood-brain barrier to enter the ischemic (but not the nonischemic) hemisphere. Whether the infarct-reducing effects of bFGF depend on intraparenchymal or intravascular mechanisms requires further study.
dc.identifier.citationJ Cereb Blood Flow Metab. 1995 Nov;15(6):953-9.
dc.identifier.contextkey492208
dc.identifier.issn0271-678X (Print)
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/neuro_pp/102
dc.identifier.pmid7593356
dc.identifier.submissionpathneuro_pp/102
dc.identifier.urihttps://hdl.handle.net/20.500.14038/37563
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7593356&dopt=Abstract ">Link to article in PubMed</a>
dc.relation.urlhttp://www.nature.com/jcbfm/journal/v15/n6/abs/jcbfm1995121a.html
dc.source.issue6
dc.source.journaltitleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
dc.source.pages953-9
dc.source.volume15
dc.subjectAnimals
dc.subjectAutoradiography
dc.subjectBlood-Brain Barrier
dc.subjectBrain
dc.subjectBrain Ischemia
dc.subjectCerebral Infarction
dc.subjectFibroblast Growth Factor 2
dc.subjectInjections, Intravenous
dc.subjectMale
dc.subjectPrecipitin Tests
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectTime Factors
dc.subjectNervous System Diseases
dc.subjectNeurology
dc.titleDelayed treatment with intravenous basic fibroblast growth factor reduces infarct size following permanent focal cerebral ischemia in rats
dc.typeJournal Article
dspace.entity.typePublication
html.description.abstract<p>Basic fibroblast growth factor (bFGF) is a polypeptide that supports the survival of brain cells (including neurons, glia, and endothelia) and protects neurons against a number of toxins and insults in vitro. This factor is also a potent dilator of cerebral pial arterioles in vivo. In previous studies, we found that intraventricularly administered bFGF reduced infarct volume in a model of focal cerebral ischemia in rats. In the current study, bFGF (45 micrograms/kg/h) in vehicle, or vehicle alone, was infused intravenously for 3 h, beginning at 30 min after permanent middle cerebral artery occlusion by intraluminal suture in mature Sprague-Dawley rats. After 24 h, neurological deficit (as assessed by a 0- to 5-point scale, with 5 = most severe) was 2.6 +/- 1.0 in vehicle-treated and 1.5 +/- 1.3 in bFGF-treated rats (mean +/- SD; N = 12 vs. 11; p = 0.009). Infarct volume was 297 +/- 65 mm3 in vehicle- and 143 +/- 135 mm3 in bFGF-treated animals (p = 0.002). During infusion, there was a modest decrease in mean arterial blood pressure but no changes in arterial blood gases or core or brain temperature in bFGF-treated rats. Autoradiography following intravenous administration of 111In-labeled bFGF showed that labeled bFGF crossed the damaged blood-brain barrier to enter the ischemic (but not the nonischemic) hemisphere. Whether the infarct-reducing effects of bFGF depend on intraparenchymal or intravascular mechanisms requires further study.</p>
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