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Regional CBF in apolipoprotein E-deficient and wild type mice during focal cerebral ischemia
R D Bart1, H Sheng, D T Laskowitz
1Department of Pediatrics, Washington University School of Medicine, St. Louis, MO, USA.
Abstract:
Apolipoprotein E-(apoE) deficient mice exhibit hypercholesterolemia, accelerated atherosclerosis and increased infarct size after middle cerebral artery occlusion (MCAO). This study examined whether worsened ischemic outcome is attributable to effects of apoE deficiency on cerebral circulation. Wild type and apoE-deficient mice underwent MCAO and autoradigraphic measurement of cerebral blood flow. Circle of Willis anatomy was examined in non-ischemic animals. Both groups exhibited similar reduction in blood flow. Both groups had 100% incidence of filling of the anterior communicating artery. The posterior communicating artery (PcomA) filled in 70% of wild type and 80% of apoE-deficient mice. Both groups had considerable variability in relative sizes of the PcmA. This study indicates that worsened outcome from MCAO of apoE-deficient mice is not attributable to any detectable vascular effects and offers validity to use of apoE-deficient mice for study of apoE as a factor in cerebral ischemic pathophysiology.
Insights
Apolipoprotein E (apoE) deficiency worsens stroke outcomes, but not due to altered cerebral blood flow or Circle of Willis anatomy. This validates apoE-deficient mice for studying apoE
Area of Science:
- Neuroscience
- Cardiovascular Science
- Genetics
Background:
- Apolipoprotein E (apoE) deficiency in mice leads to hypercholesterolemia, accelerated atherosclerosis, and larger infarcts after middle cerebral artery occlusion (MCAO).
- The precise mechanisms underlying this worsened ischemic outcome in apoE-deficient mice remain unclear.
Purpose of the Study:
- To investigate whether the exacerbated ischemic outcome in apoE-deficient mice is linked to alterations in cerebral circulation.
- To assess the role of apoE deficiency in cerebral blood flow dynamics and Circle of Willis anatomy following MCAO.
Main Methods:
- Wild-type and apoE-deficient mice underwent MCAO surgery.
- Cerebral blood flow was measured using autoradigraphy.
- Circle of Willis anatomy was analyzed in non-ischemic control animals.
Main Results:
- Both wild-type and apoE-deficient mice demonstrated similar reductions in cerebral blood flow post-MCAO.
- Anterior communicating artery filling was 100% in both groups.
- Posterior communicating artery (PcomA) filling occurred in 70% of wild-type and 80% of apoE-deficient mice, with considerable variability in PcomA size in both groups.
Conclusions:
- The worsened outcome in apoE-deficient mice after MCAO is not attributable to detectable vascular effects related to cerebral circulation.
- These findings support the use of apoE-deficient mice as a valid model for investigating the role of apoE in cerebral ischemic pathophysiology.