Document Detail

Temporal impairment of microcirculatory perfusion following focal cerebral ischemia in the spontaneously hypertensive rat.
MedLine Citation:
PMID:  9138719     Owner:  NLM     Status:  MEDLINE    
Microcirculatory impairments have theoretically been proposed as a potential factor in the development of ischemic injury, but few attempts have been made to directly assess microvascular patency following stroke. To address this issue we investigated the temporal changes in microvascular perfusion induced by permanent focal ischemia. Halothane-anesthetized spontaneously hypertensive rats were subjected to middle cerebral artery occlusion (MCAO) of 5 min to 4 h duration. Two fluorescent tracers (FITC-dextran and Evans blue) were then sequentially administered i.v. and allowed to circulate for 10 and 5 s respectively. Tissue sections were examined by fluorescent microscopy, and the mean number of perfused microvessels/mm2 calculated for cortical areas representing non-ischemic (Region A), perifocal/penumbral (Region B) and core ischemic (Region C) regions. For sham-operated controls, virtually all microvessels perfused with tracer within 5 s. In contrast MCAO induced significant reductions in the number of perfused microvessels in Regions B and C. The most marked impairments in perfusion were observed in core MCA territory (e.g. 2-10% of control values for 5 s circulation period) while, initially, the deficit was less severe in penumbral cortex. However, a secondary perfusion impairment developed over time in the perifocal/penumbral region, so that the deficit was greater 4 h after MCAO than at earlier time points (e.g. 72%, 71% and 22% of control value for 0.5, 1 and 4 h MCAO respectively; 10 s circulation period). In conclusion, MCAO induced severe impairments in microcirculatory perfusion within the core ischemic region, and to a lesser extent in the penumbra. However, the development of a more severe perfusion deficit in the penumbra within 4 h of MCAO supports the hypothesis that microcirculatory failure in this region contributes to its recruitment to the ischemic infarct.
D A Dawson; C A Ruetzler; J M Hallenbeck
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Brain research     Volume:  749     ISSN:  0006-8993     ISO Abbreviation:  Brain Res.     Publication Date:  1997 Feb 
Date Detail:
Created Date:  1997-05-06     Completed Date:  1997-05-06     Revised Date:  2003-11-14    
Medline Journal Info:
Nlm Unique ID:  0045503     Medline TA:  Brain Res     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  200-8     Citation Subset:  IM    
Stroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892-4128, USA.
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MeSH Terms
Analysis of Variance
Cerebral Arteries / pathology,  physiopathology
Cerebral Cortex / blood supply
Cerebral Infarction / pathology,  physiopathology
Cerebrovascular Circulation*
Evans Blue
Fluorescein-5-isothiocyanate / analogs & derivatives
Ischemic Attack, Transient / pathology,  physiopathology*
Microcirculation / pathology,  physiology,  physiopathology*
Rats, Inbred SHR
Time Factors
Reg. No./Substance:
0/fluorescein isothiocyanate dextran; 314-13-6/Evans Blue; 3326-32-7/Fluorescein-5-isothiocyanate; 9004-54-0/Dextrans

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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