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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 memory behavior detection. Plot graph showing changes in escape latencies in all experimental groups (A). In day 1, the escape latency was significantly longer in all ischemic groups (P<0.01) compared with sham group. In day 2, longer escape latency was found at ischemic 6-week group (P<0.01). In day 3 and day 4, the escape latency was significantly prolonged at 2- and 4-week groups (P<0.05), and 6-week group (P<0.01) after bilateral common carotid artery occlusion (BCCAO). The travel path of rats crossing the platform (circle) or platform quadrant was shown in (B). Quantitative data showed that the frequency crossing the original platform was decreased in all ischemic groups (C). And the duration travelling in the original platform quadrant was also declined in ischemic groups (P<0.05 at 2 weeks, P<0.01 at 4 and 6 weeks after BCCAO) (D). **P<0.01; *P<0.05, compared with sham.
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fig7: Changes in memory behavior detection. Plot graph showing changes in escape latencies in all experimental groups (A). In day 1, the escape latency was significantly longer in all ischemic groups (P<0.01) compared with sham group. In day 2, longer escape latency was found at ischemic 6-week group (P<0.01). In day 3 and day 4, the escape latency was significantly prolonged at 2- and 4-week groups (P<0.05), and 6-week group (P<0.01) after bilateral common carotid artery occlusion (BCCAO). The travel path of rats crossing the platform (circle) or platform quadrant was shown in (B). Quantitative data showed that the frequency crossing the original platform was decreased in all ischemic groups (C). And the duration travelling in the original platform quadrant was also declined in ischemic groups (P<0.05 at 2 weeks, P<0.01 at 4 and 6 weeks after BCCAO) (D). **P<0.01; *P<0.05, compared with sham.

Mentions: After we found that CCH induced neuronal degeneration, we further investigated whether two-step BCCAO model in our study would induce cognitive impairment. Rats were trained to perform Morris water maze. In the first learning trial (Figure 7A), the escape latency in the sham group was 36.2±2.5 seconds in day 1. After surgery, it significantly prolonged to 48.3±2.7 seconds , 53.0±1.9 seconds, and 54.7±2.2 seconds at 2, 4, and 6 weeks after BCCAO, all P<0.01 compared with sham. In day 2, although there was no difference between the sham, postischemic 2- and 4-week groups, the escape latency was prolong in ischemic 6-week group, P<0.01 versus sham. In day 3, the escape latency was 32.5±2.9 seconds at ischemic 2-week group (P<0.05), 33.1±1 seconds (P<0.05) at ischemic 4-week group and 42.3±2.4 seconds (P<0.01) at ischemic 6-week group, compared with sham (24.3±4.6 seconds ). The record of escape latency in day 4 was similar to day 3.


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 memory behavior detection. Plot graph showing changes in escape latencies in all experimental groups (A). In day 1, the escape latency was significantly longer in all ischemic groups (P<0.01) compared with sham group. In day 2, longer escape latency was found at ischemic 6-week group (P<0.01). In day 3 and day 4, the escape latency was significantly prolonged at 2- and 4-week groups (P<0.05), and 6-week group (P<0.01) after bilateral common carotid artery occlusion (BCCAO). The travel path of rats crossing the platform (circle) or platform quadrant was shown in (B). Quantitative data showed that the frequency crossing the original platform was decreased in all ischemic groups (C). And the duration travelling in the original platform quadrant was also declined in ischemic groups (P<0.05 at 2 weeks, P<0.01 at 4 and 6 weeks after BCCAO) (D). **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

fig7: Changes in memory behavior detection. Plot graph showing changes in escape latencies in all experimental groups (A). In day 1, the escape latency was significantly longer in all ischemic groups (P<0.01) compared with sham group. In day 2, longer escape latency was found at ischemic 6-week group (P<0.01). In day 3 and day 4, the escape latency was significantly prolonged at 2- and 4-week groups (P<0.05), and 6-week group (P<0.01) after bilateral common carotid artery occlusion (BCCAO). The travel path of rats crossing the platform (circle) or platform quadrant was shown in (B). Quantitative data showed that the frequency crossing the original platform was decreased in all ischemic groups (C). And the duration travelling in the original platform quadrant was also declined in ischemic groups (P<0.05 at 2 weeks, P<0.01 at 4 and 6 weeks after BCCAO) (D). **P<0.01; *P<0.05, compared with sham.
Mentions: After we found that CCH induced neuronal degeneration, we further investigated whether two-step BCCAO model in our study would induce cognitive impairment. Rats were trained to perform Morris water maze. In the first learning trial (Figure 7A), the escape latency in the sham group was 36.2±2.5 seconds in day 1. After surgery, it significantly prolonged to 48.3±2.7 seconds , 53.0±1.9 seconds, and 54.7±2.2 seconds at 2, 4, and 6 weeks after BCCAO, all P<0.01 compared with sham. In day 2, although there was no difference between the sham, postischemic 2- and 4-week groups, the escape latency was prolong in ischemic 6-week group, P<0.01 versus sham. In day 3, the escape latency was 32.5±2.9 seconds at ischemic 2-week group (P<0.05), 33.1±1 seconds (P<0.05) at ischemic 4-week group and 42.3±2.4 seconds (P<0.01) at ischemic 6-week group, compared with sham (24.3±4.6 seconds ). The record of escape latency in day 4 was similar to day 3.

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