Two-photon microscopic measurements of the effect of bilateral carotid artery stenosis on the cerebral and retinal microcirculation

2021 ◽  
Author(s):  
Baoqiang Li ◽  
Ikbal Sencan ◽  
Hajime Takase ◽  
Ji Leng ◽  
Mohammed Alfadhel ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Carotid Artery Stenosis ◽  
Artery Stenosis ◽  
Two Photon ◽  
Bilateral Carotid ◽  
Retinal Microcirculation ◽  
Bilateral Carotid Artery

Multiple encephalogaleoperiosteal synangiosis for bilateral carotid artery stenosis in a 13-year-old girl: a case report

2015 ◽  
Vol 32 (5) ◽  
pp. 877-880 ◽  
Author(s):  
Akinori Inamura ◽  
Sadahiro Nomura ◽  
Hirokazu Sadahiro ◽  
Takayuki Oku ◽  
Hideyuki Ishihara ◽  
...  
Keyword(s):  
Case Report ◽  
Carotid Artery ◽  
Carotid Artery Stenosis ◽  
Artery Stenosis ◽  
Bilateral Carotid ◽  
Bilateral Carotid Artery

Abstract TP434: Mouse Bilateral Carotid Artery Stenosis Leads to Unexpected Early Changes in Blood-Brain Barrier Integrity

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Jill Roberts ◽  
Michael Maniskas ◽  
Gregory Bix
Keyword(s):  
White Matter ◽  
Carotid Artery ◽  
Blood Brain Barrier ◽  
Carotid Artery Stenosis ◽  
Artery Stenosis ◽  
Brain Barrier ◽  
Brain White Matter ◽  
Blood Brain ◽  
Bilateral Carotid ◽  
Bilateral Carotid Artery

Bilateral carotid artery stenosis (BCAS) is one experimental model of vascular dementia that is thought to preferentially impact brain white matter. Indeed, it is generally accepted that hippocampal and cortical pathology is not observed prior to 30 days post-injury. Since changes in the blood-brain barrier (BBB) permeability are known to precede more overt brain pathology in a variety of diseases, we hypothesized that BBB changes could occur earlier after BCAS in the hippocampus, striatum and cortex and be a precursor of longer term pathology in these regions. In our study, 3 month old male C57/Bl6 mice underwent BCAS with 0.18 mm coils or sham surgery control and changes in BBB were analyzed by collagen IV (vascular basement membrane component), claudin-5 and occludin (tight junction proteins), Evan’s blue (permeability marker), and Ki-67 (marker of cell proliferation) immunohistochemistry, protein and RNA expression levels after 3, 7, 14, or 21 days. Surprisingly, significant changes in markers of cerebrovascular integrity were detected within 7 days compared to sham animals, not only in the striatum but also in the hippocampus. Increased astrocyte and microglia activation was also observed in these regions and TUNEL staining also indicates cell death in the hippocampus within 7 days. While few changes were observed in the cortex, some of the animals did experience cortical ischemic infarcts within 14 days. In conclusion, this study demonstrates for the first time that changes in the BBB occur shortly after BCAS in multiple regions throughout the brain and suggests that such changes might underlie the gradual development of BCAS non-white matter pathology.

Abstract WP426: Early Non-white Matter Changes in Cerebrovascular Integrity in Mouse Brain Following Bilateral Carotid Artery Stenosis

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Jill Roberts ◽  
Michael Maniskas ◽  
Gregory J Bix
Keyword(s):  
White Matter ◽  
Carotid Artery ◽  
Carotid Artery Stenosis ◽  
Collagen Iv ◽  
Artery Stenosis ◽  
Ki 67 ◽  
Tomato Lectin ◽  
Bilateral Carotid ◽  
White Matter Pathology ◽  
Bilateral Carotid Artery

Bilateral carotid artery stenosis (BCAS) is an experimental model of vascular dementia which leads to white matter lesions and cognitive dysfunction in mice. Unfortunately, with time the white matter pathology worsens and spreads to the hippocampus and cortex. While some variability in the temporal and spatial distribution of brain injury may result from inter-mouse strain differences in cerebrovascular anatomy, coil size employed to constrict the carotids and surgical technique, it is generally accepted that hippocampal, striatal and cortical pathology is not significantly present prior to 30 days. However, as changes in cerebrovascular integrity, i.e. blood-brain barrier (BBB) permeability, are known to precede more overt brain pathology in stroke, we hypothesized that BBB changes could occur earlier after BCAS in the hippocampus, striatum and cortex and be a precursor of longer term pathology in these regions. In our study, 3 month old male C57/Bl6 mice underwent BCAS with 0.18 mm coils or sham surgery control and cerebrovascular integrity was analyzed by collagen IV (vascular basement membrane component), tomato-lectin (marker of endothelial cells) and Ki-67 (marker of cell proliferation) immunohistochemistry after 7, 14, or 21 days (n=4 animals per group per day). By day 14 we noted that collagen IV staining density was significantly less in the hippocampus compared to sham controls. Surprisingly, both collagen IV and tomato-lectin staining pattern indicate blood vessel disruption in not only the hippocampus but the striatum as well. Expression of Ki-67 increased in both of these regions, and further co-labeling studies will shed light on cell specificity. Similar differences were noted at all days tested, with few changes observed in the cortex. In conclusion, this study demonstrates for the first time that changes in cerebrovascular integrity occur earlier than expected after BCAS and suggests that such changes might underlie the gradual development of BCAS non-white matter pathology.

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