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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

Morphologic changes in microvessels. Micrograph showing CD34 immunofluorescence staining of microvessels in the parietal cortex, striatum, and cerebellum at different points after bilateral common carotid artery occlusion (BCCAO) (A). In the sham group, stronger staining of CD34-positive microvessels was seen in the parietal cortex (A- and F, arrows), striatum (A1 and F1, arrows) and cerebellum (A2 and F2, arrows). However, the staining signal reduced at 2 weeks (B-, G, B1, G1, B2, G2) and 3 weeks (C-, H, C1, H1, C2, H2) in these three areas, and 4 weeks (D-, I, D1, I1) after BCCAO in the parietal cortex and the striatum. Stronger labelled CD34-positive microvessels reappeared earlier in the cerebellum at 4 weeks (D2, I2) and later at 6 weeks (E-, J, E1, J1, E2, J2) in the parietal cortex and the striatum after BCCAO. LPC, left parietal cortex; RPC, right parietal cortex; LST, left striatum; RST, right striatum; LCB, left cerebellum; RCB, right cerebellum. Histogram showing quantitative data (B–D): In the left parietal cortex, the percentage of the number and areas of microvessels decreased at 2, 3, and 4 weeks (P<0.01) and returned to the sham level at 6 wk (P>0.05). (B) In the right parietal cortex, the percentage of the number and areas of microvessels also decreased at 2, 3, and 4 weeks (P<0.01 and P<0.05) but increased at 6 weeks after BCCAO (RMVN, P<0.01 and RMVD, P<0.05) compared with the sham group. The percentage of the number and areas of microvessels in the striatum underwent a similar changing pattern (C). In the cerebellum, however, the percentage of the number and areas of microvessels decreased at 2 and 3 weeks but returned to the sham level from 4 weeks after BCCAO (D). LMVN, the number of microvessels in the left side; LMVD, the area of microvessels in the left side. RMVN, the number of microvessels in the right side; RMVD, the area of microvessels in the right side. **P<0.01; *P<0.05 compared with sham. Scale bar, 20 μm.
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fig3: Morphologic changes in microvessels. Micrograph showing CD34 immunofluorescence staining of microvessels in the parietal cortex, striatum, and cerebellum at different points after bilateral common carotid artery occlusion (BCCAO) (A). In the sham group, stronger staining of CD34-positive microvessels was seen in the parietal cortex (A- and F, arrows), striatum (A1 and F1, arrows) and cerebellum (A2 and F2, arrows). However, the staining signal reduced at 2 weeks (B-, G, B1, G1, B2, G2) and 3 weeks (C-, H, C1, H1, C2, H2) in these three areas, and 4 weeks (D-, I, D1, I1) after BCCAO in the parietal cortex and the striatum. Stronger labelled CD34-positive microvessels reappeared earlier in the cerebellum at 4 weeks (D2, I2) and later at 6 weeks (E-, J, E1, J1, E2, J2) in the parietal cortex and the striatum after BCCAO. LPC, left parietal cortex; RPC, right parietal cortex; LST, left striatum; RST, right striatum; LCB, left cerebellum; RCB, right cerebellum. Histogram showing quantitative data (B–D): In the left parietal cortex, the percentage of the number and areas of microvessels decreased at 2, 3, and 4 weeks (P<0.01) and returned to the sham level at 6 wk (P>0.05). (B) In the right parietal cortex, the percentage of the number and areas of microvessels also decreased at 2, 3, and 4 weeks (P<0.01 and P<0.05) but increased at 6 weeks after BCCAO (RMVN, P<0.01 and RMVD, P<0.05) compared with the sham group. The percentage of the number and areas of microvessels in the striatum underwent a similar changing pattern (C). In the cerebellum, however, the percentage of the number and areas of microvessels decreased at 2 and 3 weeks but returned to the sham level from 4 weeks after BCCAO (D). LMVN, the number of microvessels in the left side; LMVD, the area of microvessels in the left side. RMVN, the number of microvessels in the right side; RMVD, the area of microvessels in the right side. **P<0.01; *P<0.05 compared with sham. Scale bar, 20 μm.

Mentions: To investigate whether angiogenesis may be activated after BCCAO, we used CD34 (an endothelial cell marker) immunofluorescence to detect changes in microvessels in the parietal cortex, striatum, and cerebellum (Figure 3A, 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)

Morphologic changes in microvessels. Micrograph showing CD34 immunofluorescence staining of microvessels in the parietal cortex, striatum, and cerebellum at different points after bilateral common carotid artery occlusion (BCCAO) (A). In the sham group, stronger staining of CD34-positive microvessels was seen in the parietal cortex (A- and F, arrows), striatum (A1 and F1, arrows) and cerebellum (A2 and F2, arrows). However, the staining signal reduced at 2 weeks (B-, G, B1, G1, B2, G2) and 3 weeks (C-, H, C1, H1, C2, H2) in these three areas, and 4 weeks (D-, I, D1, I1) after BCCAO in the parietal cortex and the striatum. Stronger labelled CD34-positive microvessels reappeared earlier in the cerebellum at 4 weeks (D2, I2) and later at 6 weeks (E-, J, E1, J1, E2, J2) in the parietal cortex and the striatum after BCCAO. LPC, left parietal cortex; RPC, right parietal cortex; LST, left striatum; RST, right striatum; LCB, left cerebellum; RCB, right cerebellum. Histogram showing quantitative data (B–D): In the left parietal cortex, the percentage of the number and areas of microvessels decreased at 2, 3, and 4 weeks (P<0.01) and returned to the sham level at 6 wk (P>0.05). (B) In the right parietal cortex, the percentage of the number and areas of microvessels also decreased at 2, 3, and 4 weeks (P<0.01 and P<0.05) but increased at 6 weeks after BCCAO (RMVN, P<0.01 and RMVD, P<0.05) compared with the sham group. The percentage of the number and areas of microvessels in the striatum underwent a similar changing pattern (C). In the cerebellum, however, the percentage of the number and areas of microvessels decreased at 2 and 3 weeks but returned to the sham level from 4 weeks after BCCAO (D). LMVN, the number of microvessels in the left side; LMVD, the area of microvessels in the left side. RMVN, the number of microvessels in the right side; RMVD, the area of microvessels in the right side. **P<0.01; *P<0.05 compared with sham. Scale bar, 20 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig3: Morphologic changes in microvessels. Micrograph showing CD34 immunofluorescence staining of microvessels in the parietal cortex, striatum, and cerebellum at different points after bilateral common carotid artery occlusion (BCCAO) (A). In the sham group, stronger staining of CD34-positive microvessels was seen in the parietal cortex (A- and F, arrows), striatum (A1 and F1, arrows) and cerebellum (A2 and F2, arrows). However, the staining signal reduced at 2 weeks (B-, G, B1, G1, B2, G2) and 3 weeks (C-, H, C1, H1, C2, H2) in these three areas, and 4 weeks (D-, I, D1, I1) after BCCAO in the parietal cortex and the striatum. Stronger labelled CD34-positive microvessels reappeared earlier in the cerebellum at 4 weeks (D2, I2) and later at 6 weeks (E-, J, E1, J1, E2, J2) in the parietal cortex and the striatum after BCCAO. LPC, left parietal cortex; RPC, right parietal cortex; LST, left striatum; RST, right striatum; LCB, left cerebellum; RCB, right cerebellum. Histogram showing quantitative data (B–D): In the left parietal cortex, the percentage of the number and areas of microvessels decreased at 2, 3, and 4 weeks (P<0.01) and returned to the sham level at 6 wk (P>0.05). (B) In the right parietal cortex, the percentage of the number and areas of microvessels also decreased at 2, 3, and 4 weeks (P<0.01 and P<0.05) but increased at 6 weeks after BCCAO (RMVN, P<0.01 and RMVD, P<0.05) compared with the sham group. The percentage of the number and areas of microvessels in the striatum underwent a similar changing pattern (C). In the cerebellum, however, the percentage of the number and areas of microvessels decreased at 2 and 3 weeks but returned to the sham level from 4 weeks after BCCAO (D). LMVN, the number of microvessels in the left side; LMVD, the area of microvessels in the left side. RMVN, the number of microvessels in the right side; RMVD, the area of microvessels in the right side. **P<0.01; *P<0.05 compared with sham. Scale bar, 20 μm.
Mentions: To investigate whether angiogenesis may be activated after BCCAO, we used CD34 (an endothelial cell marker) immunofluorescence to detect changes in microvessels in the parietal cortex, striatum, and cerebellum (Figure 3A, 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