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Chronic cerebral hypoperfusion induces vascular plasticity and hemodynamics but also neuronal degeneration and cognitive impairment.

Jing Z, Shi C, Zhu L, Xiang Y, Chen P, Xiong Z, Li W, Ruan Y, Huang L - J. Cereb. Blood Flow Metab. (2015)

Bottom Line: The CBF of the cortex, striatum, and cerebellum dramatically decreased after right common carotid artery occlusion (RCCAO), and remained lower level at 2 weeks after BCCAO.Neuronal degeneration occurred in the cortex and striatum from 2 to 6 weeks, but the number of glial cells dramatically increased at 4 weeks after BCCAO.Our results suggest that CCH induces a compensative mechanism attempting to maintain optimal CBF to the brain.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, The First Affiliated Hospital, Jinan University, Guangzhou, China.

ABSTRACT
Chronic cerebral hypoperfusion (CCH) induces cognitive impairment, but the compensative mechanism of cerebral blood flow (CBF) is not fully understood. The present study mainly investigated dynamic changes in CBF, angiogenesis, and cellular pathology in the cortex, the striatum, and the cerebellum, and also studied cognitive impairment of rats induced by bilateral common carotid artery occlusion (BCCAO). Magnetic resonance imaging (MRI) techniques, immunochemistry, and Morris water maze were employed to the study. The CBF of the cortex, striatum, and cerebellum dramatically decreased after right common carotid artery occlusion (RCCAO), and remained lower level at 2 weeks after BCCAO. It returned to the sham level from 3 to 6 weeks companied by the dilation of vertebral arteries after BCCAO. The number of microvessels declined at 2, 3, and 4 weeks but increased at 6 weeks after BCCAO. Neuronal degeneration occurred in the cortex and striatum from 2 to 6 weeks, but the number of glial cells dramatically increased at 4 weeks after BCCAO. Cognitive impairment of ischemic rats was directly related to ischemic duration. Our results suggest that CCH induces a compensative mechanism attempting to maintain optimal CBF to the brain. However, this limited compensation cannot prevent neuronal loss and cognitive impairment after permanent ischemia.

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Related in: MedlinePlus

Changes in bilateral common carotid arteries (CCAs) and vertebral arteries (VAs) before and after bilateral common carotid artery occlusion (BCCAO). Three-dimensional time-of-flight MR angiography (3D TOF-MRA) images showing morphologic changes of CCAs and VAs (A). In pre-occlusion rats, bilateral CCAs were clearly seen (A-, arrows). After RCCA was occluded, its signal disappeared from the image (B-, arrow head), but LCCA was still visible (B-, arrow). After BCCAO, both CCA signals were absent from the image (C-, arrow head). At the same time, bead-like VAs were seen (C-, arrows). Gradual enlargement of VAs was observed from 2 to 6 weeks after BCCAO (D-, E-, and F-, arrows). Histogram showing changes in diameter and area of bilateral VAs (B, C). There was no difference in diameter and area of VAs between pre-occlusion group and right common carotid artery occlusion (RCCAO) group. The diameter of both VAs increased at 1 week after RCCAO when BCCAO was induced (P<0.01 versus RCCAO group in the left VA, P<0.01 versus the pre-occlusion and RCCAO groups in the right VA). VAs gradually became larger from 2, 3, and 4 weeks, and peaked at 6 weeks after BCCAO. Changes in VA area also underwent a similar pattern as that for VA diameter after BCCAO. **P<0.01; *P<0.05 compared with sham.
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fig2: Changes in bilateral common carotid arteries (CCAs) and vertebral arteries (VAs) before and after bilateral common carotid artery occlusion (BCCAO). Three-dimensional time-of-flight MR angiography (3D TOF-MRA) images showing morphologic changes of CCAs and VAs (A). In pre-occlusion rats, bilateral CCAs were clearly seen (A-, arrows). After RCCA was occluded, its signal disappeared from the image (B-, arrow head), but LCCA was still visible (B-, arrow). After BCCAO, both CCA signals were absent from the image (C-, arrow head). At the same time, bead-like VAs were seen (C-, arrows). Gradual enlargement of VAs was observed from 2 to 6 weeks after BCCAO (D-, E-, and F-, arrows). Histogram showing changes in diameter and area of bilateral VAs (B, C). There was no difference in diameter and area of VAs between pre-occlusion group and right common carotid artery occlusion (RCCAO) group. The diameter of both VAs increased at 1 week after RCCAO when BCCAO was induced (P<0.01 versus RCCAO group in the left VA, P<0.01 versus the pre-occlusion and RCCAO groups in the right VA). VAs gradually became larger from 2, 3, and 4 weeks, and peaked at 6 weeks after BCCAO. Changes in VA area also underwent a similar pattern as that for VA diameter after BCCAO. **P<0.01; *P<0.05 compared with sham.

Mentions: To investigate whether VAs morphologically changed after BCCAO, we used an MRA technique to measure diameters of VAs. Morphologic changes of VAs in different groups were shown in Figure 2A. Both CCAs were clearly seen in pre-occlusion group (Figure 2A-, arrows). After RCCAO, the RCCA signal disappeared (Figure 2B-, arrow head), while the LCCA was still visible (Figure 2B-, arrow). After BCCAO, both CCA signals were absent, but both VAs were still seen (Figure 2C-, arrows). From 2 to 6 weeks after BCCAO, VA diameter gradually enlarged (Figure 2D-, E- & G-, arrows).


Chronic cerebral hypoperfusion induces vascular plasticity and hemodynamics but also neuronal degeneration and cognitive impairment.

Jing Z, Shi C, Zhu L, Xiang Y, Chen P, Xiong Z, Li W, Ruan Y, Huang L - J. Cereb. Blood Flow Metab. (2015)

Changes in bilateral common carotid arteries (CCAs) and vertebral arteries (VAs) before and after bilateral common carotid artery occlusion (BCCAO). Three-dimensional time-of-flight MR angiography (3D TOF-MRA) images showing morphologic changes of CCAs and VAs (A). In pre-occlusion rats, bilateral CCAs were clearly seen (A-, arrows). After RCCA was occluded, its signal disappeared from the image (B-, arrow head), but LCCA was still visible (B-, arrow). After BCCAO, both CCA signals were absent from the image (C-, arrow head). At the same time, bead-like VAs were seen (C-, arrows). Gradual enlargement of VAs was observed from 2 to 6 weeks after BCCAO (D-, E-, and F-, arrows). Histogram showing changes in diameter and area of bilateral VAs (B, C). There was no difference in diameter and area of VAs between pre-occlusion group and right common carotid artery occlusion (RCCAO) group. The diameter of both VAs increased at 1 week after RCCAO when BCCAO was induced (P<0.01 versus RCCAO group in the left VA, P<0.01 versus the pre-occlusion and RCCAO groups in the right VA). VAs gradually became larger from 2, 3, and 4 weeks, and peaked at 6 weeks after BCCAO. Changes in VA area also underwent a similar pattern as that for VA diameter after BCCAO. **P<0.01; *P<0.05 compared with sham.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4528009&req=5

fig2: Changes in bilateral common carotid arteries (CCAs) and vertebral arteries (VAs) before and after bilateral common carotid artery occlusion (BCCAO). Three-dimensional time-of-flight MR angiography (3D TOF-MRA) images showing morphologic changes of CCAs and VAs (A). In pre-occlusion rats, bilateral CCAs were clearly seen (A-, arrows). After RCCA was occluded, its signal disappeared from the image (B-, arrow head), but LCCA was still visible (B-, arrow). After BCCAO, both CCA signals were absent from the image (C-, arrow head). At the same time, bead-like VAs were seen (C-, arrows). Gradual enlargement of VAs was observed from 2 to 6 weeks after BCCAO (D-, E-, and F-, arrows). Histogram showing changes in diameter and area of bilateral VAs (B, C). There was no difference in diameter and area of VAs between pre-occlusion group and right common carotid artery occlusion (RCCAO) group. The diameter of both VAs increased at 1 week after RCCAO when BCCAO was induced (P<0.01 versus RCCAO group in the left VA, P<0.01 versus the pre-occlusion and RCCAO groups in the right VA). VAs gradually became larger from 2, 3, and 4 weeks, and peaked at 6 weeks after BCCAO. Changes in VA area also underwent a similar pattern as that for VA diameter after BCCAO. **P<0.01; *P<0.05 compared with sham.
Mentions: To investigate whether VAs morphologically changed after BCCAO, we used an MRA technique to measure diameters of VAs. Morphologic changes of VAs in different groups were shown in Figure 2A. Both CCAs were clearly seen in pre-occlusion group (Figure 2A-, arrows). After RCCAO, the RCCA signal disappeared (Figure 2B-, arrow head), while the LCCA was still visible (Figure 2B-, arrow). After BCCAO, both CCA signals were absent, but both VAs were still seen (Figure 2C-, arrows). From 2 to 6 weeks after BCCAO, VA diameter gradually enlarged (Figure 2D-, E- & G-, arrows).

Bottom Line: The CBF of the cortex, striatum, and cerebellum dramatically decreased after right common carotid artery occlusion (RCCAO), and remained lower level at 2 weeks after BCCAO.Neuronal degeneration occurred in the cortex and striatum from 2 to 6 weeks, but the number of glial cells dramatically increased at 4 weeks after BCCAO.Our results suggest that CCH induces a compensative mechanism attempting to maintain optimal CBF to the brain.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, The First Affiliated Hospital, Jinan University, Guangzhou, China.

ABSTRACT
Chronic cerebral hypoperfusion (CCH) induces cognitive impairment, but the compensative mechanism of cerebral blood flow (CBF) is not fully understood. The present study mainly investigated dynamic changes in CBF, angiogenesis, and cellular pathology in the cortex, the striatum, and the cerebellum, and also studied cognitive impairment of rats induced by bilateral common carotid artery occlusion (BCCAO). Magnetic resonance imaging (MRI) techniques, immunochemistry, and Morris water maze were employed to the study. The CBF of the cortex, striatum, and cerebellum dramatically decreased after right common carotid artery occlusion (RCCAO), and remained lower level at 2 weeks after BCCAO. It returned to the sham level from 3 to 6 weeks companied by the dilation of vertebral arteries after BCCAO. The number of microvessels declined at 2, 3, and 4 weeks but increased at 6 weeks after BCCAO. Neuronal degeneration occurred in the cortex and striatum from 2 to 6 weeks, but the number of glial cells dramatically increased at 4 weeks after BCCAO. Cognitive impairment of ischemic rats was directly related to ischemic duration. Our results suggest that CCH induces a compensative mechanism attempting to maintain optimal CBF to the brain. However, this limited compensation cannot prevent neuronal loss and cognitive impairment after permanent ischemia.

Show MeSH
Related in: MedlinePlus