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Bilateral internal carotid arteries ligation temporary impairs brain vasculaturev in young rats
Abstract Bilateral internal carotid artery ligation (BICL) rat model is one of the chronic cerebral hypoperfusion animal models used for investigating brain dysfunction related diseases. Cerebral blood flow decreases in different cerebral regions in a time-dependent manner after the BICL. However li...
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Published in: | Autonomic neuroscience 2013-01, Vol.173 (1), p.39-44 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Abstract Bilateral internal carotid artery ligation (BICL) rat model is one of the chronic cerebral hypoperfusion animal models used for investigating brain dysfunction related diseases. Cerebral blood flow decreases in different cerebral regions in a time-dependent manner after the BICL. However little is known about the cerebral vasculature change in the brain after the BICL. In the current study, the bilateral internal carotid arteries of the juvenile rats were permanently ligated and the change of the cerebral vasculature was studied 7, 14 and 21 days after the BICL. In the juvenile rats, 7 days after the BICL, the functional vascular area was decreased significantly in the anterior half of the cerebral cortex, but it had only little decrease in the posterior half of the cerebral cortex and hippocampus. However, at the time points of 14 and 21 days after the surgery, the functional vascular area throughout the whole cerebral cortex and hippocampus was almost similar to those in the sham control rats. In conclusion, the results from our current study showed that in the BICL hypoperfusion model in young rats, the brain functional vascular area was impaired initially in certain brain regions after the artery ligation, but likely to be quickly self-recovered late after. The results suggest that the brain vasculature in young rats has plasticity to external insult caused by cerebral hypoperfusion. |
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ISSN: | 1566-0702 1872-7484 |
DOI: | 10.1016/j.autneu.2012.11.003 |