Cognitive functions of carotid artery stenosis in the aged rat

Zhou, Zhenhua; Zhang, Y; Zhu, Chuhong; Sui, Jian-feng; Wu, Guohao; Meng, Ziqi; Huang, Heqing; Chen, Kang

doi:10.1016/j.neuroscience.2012.05.060

Cited by 16 publications

(19 citation statements)

References 36 publications

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Section: Resultsmentioning

confidence: 99%

“…Binding stainless microtube with different diameter to bilateral carotid artery could produce mild, moderate and heavy carotid stenosis in rats [5]. Angiography demonstrated that a microtube with a diameter of 0.45 mm could lead to heavy carotid stenosis (the inner diameter of carotid artery <70%) when it was bound to carotid artery [5]. Thus, as described previously, we used such microtubes in this study to produce heavy carotid stenosis in rats to imitate similar conditions in humans, and examined the destiny of hippocampus CA1 neurons treated with or without ischemic postconditioning before carotid stenosis was relieved.…”

Section: Resultsmentioning

confidence: 99%

“…Given that hypoperfusion due to long periods of heavy carotid stenosis could result in neuronal injury in CA region at day 30 [5], we measured the changes of cerebral blood flow prior to and after relief of carotid stenosis. We found that the cerebral blood flow recovered from 45% at 3 days of carotid stenosis to 78% at day 4 when heavy carotid stenosis was relieved, which was consistent with previous findings [7].…”

Section: Resultsmentioning

confidence: 99%

“…Clinical studies have also shown that patients with carotid stenosis would have cognition dysfunction due to long-term cerebral hypoperfusion [3,4]. Animal study demonstrated that almost 50% of the neurons in rat hippocampus CA1 region would die at 30 days when severe bilateral carotid artery stenosis was produced [5]. By contrast, clinical observations and animal experiments demonstrated that the damaged neurological function would be improved when carotid stenosis was relieved [6,7].…”

Section: Introductionmentioning

confidence: 99%

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Ischemic Postconditioning Alleviates Neuronal Injury Caused by Relief of Carotid Stenosis in a Rat Model of Cerebral Hypoperfusion

Feng

Luo

et al. 2012

IJMS

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The effects of early relief of heavy bilateral carotid stenosis and ischemic postconditioning on hippocampus CA1 neurons are still unclear. In this study, we used a rat model to imitate severe bilateral carotid stenosis in humans. The rats were divided into sham group, carotid stenosis group, stenosis relief group and ischemic postconditioning group. Ischemic postconditioning consisted of three cycles of 30 s ischemia and 30 s reperfusion. The cerebral blood flow was measured with a laser Doppler flowmeter. Neuronal death in the CA1 region was observed by hematoxylin-eosin staining, and the number of live neurons was assessed by cell counting under a light microscope. The levels of oxidative products MDA and 8-iso-PGF2α, inflammatory factors IL-1β and TNF-α, and the activities of anti-oxidative enzymes SOD and CAT were assayed by specific enzyme-linked immunosorbent assay (ELISA) kits, respectively. We found that relief of carotid stenosis and ischemic postconditioning could increase cerebral blood flow. When stenosis was relieved, the percentage of live neurons was 66.6% ± 6.2% on day 3 and 62.3% ± 9.8% on day 27, which was significantly higher than 55.5% ± 4.8% in stenosis group. Ischemic postconditioning markedly improved the live neurons to 92.5% ± 6.7% on day 3 and 88.6% ± 9.1% on day 27. Further study showed that, neuronal death caused by relief of stenosis is associated with increased oxidative stress and enhanced inflammatory response, and the protection of ischemic postconditioning is related to inhibition of oxidative stress and suppression of inflammatory response.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Ischemic Postconditioning Alleviates Neuronal Injury Caused by Relief of Carotid Stenosis in a Rat Model of Cerebral Hypoperfusion

Feng

Luo

et al. 2012

IJMS

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“…Cerebral artery stenosis is not only an important risk factor for ischemic cerebrovascular diseases, but is also closely related to cognitive disorders [17,18]. There is evidence [19] that cerebral artery stenosis is a major cause of chronic hypoperfusion.…”

Section: Discussionmentioning

confidence: 99%

Influence of stent-assisted angioplasty on cognitive function and affective disorder in elderly patients with symptomatic vertebrobasilar artery stenosis

et al. 2014

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BackgroundWe aimed to investigate cognitive function and affective disorder in elderly patients with symptomatic vertebrobasilar artery stenosis (SVAS) after stent-assisted angioplasty (SAA) and to explore the potential mechanism.Material/MethodsThe study subjects were 26 elderly SVAS patients who were non-responsive to pharmacotherapy and received SAA (study group) and 30 patients receiving intracoronary stent implantation (control group). Montreal cognitive assessment (MoCA), Hamilton depression rating scale (HAMD), and Hamilton anxiety rating scale (HAMA) were used.ResultsThe total MoCA score, scores of line connection, copying cube, drawing clock, and delayed recall increased significantly in the study group after surgery (P<0.05, P<0.01). In addition, the MoCA score increased over time and the total MoCA score at 12 months was markedly higher than that at 1 month (P<0.05). The scores of HAMD and HAMA decreased dramatically after surgery compared with before surgery in these patients (P<0.01). A comparison at the corresponding period was performed between study group and control group, and it was found that the differences in total MoCA scores and scores of line connection, copying cube, drawing clock, and delayed recall before surgery and at 1 month after surgery were significant (P<0.05, P<0.01).ConclusionsSAA may improve the visuospatial/executive abilities and delayed recall, as well as the depression and anxiety in patients with SVAS. Larger and controlled trails are needed to investigate the effect of SAA on cognition and affection in these patients.

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Effect of a Rho Kinase Inhibitor on Cognitive Impairment Induced by Chronic Cerebral Hypoperfusion in Rats

2015

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We examined the efficacy of a Rho kinase inhibitor, Fasudil, on cognitive impairment induced by chronic cerebral hypoperfusion in rats. Thirty-two male adult Sprague-Dawley rats were randomly divided into three groups; treated (T), control (C), and sham-operated (Sh); severe stenosis of the carotid arteries was modeled in the former two groups. During two weeks, 8.35 mg/kg Fasudil and physiological saline were i.p. applied twice per day in the T and C groups, respectively. The Morris water maze test was performed in each group to detect changes in the cognitive function and to observe pathological shifts in hippocampal morphology in rats after eight weeks. The mean escape latency was distinctly shorter (P < 0.01), and the percentage of swimming distance within the platform quadrant was significantly greater (P < 0.01) in the T group, compared to those in the C group at the corresponding time points. The rate of carotid artery stenosis in rats demonstrated no statistical difference between the T and C groups (P > 0.05). Fasudil injections effectively normalized hippocampal pathomorphology in the T group. Thus, the Rho kinase inhibitor obviously ameliorated cognitive impairment induced by chronic cerebral hypoperfusion in rats.

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Cognitive functions of carotid artery stenosis in the aged rat

Cited by 16 publications

References 36 publications

Ischemic Postconditioning Alleviates Neuronal Injury Caused by Relief of Carotid Stenosis in a Rat Model of Cerebral Hypoperfusion

Ischemic Postconditioning Alleviates Neuronal Injury Caused by Relief of Carotid Stenosis in a Rat Model of Cerebral Hypoperfusion

Influence of stent-assisted angioplasty on cognitive function and affective disorder in elderly patients with symptomatic vertebrobasilar artery stenosis

Effect of a Rho Kinase Inhibitor on Cognitive Impairment Induced by Chronic Cerebral Hypoperfusion in Rats

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