Capillary Remodeling and Collateral Growth Without Angiogenesis After Unilateral Common Carotid Artery Occlusion in Mice

Guo, Huailian; Itoh, Yoshiaki; Toriumi, Haruki; Yamada, Satoshi; Tsutsumi, Yutaka; Hoshino, Haruhiko; Suzuki, Noriyuki

doi:10.1111/j.1549-8719.2011.00081.x

Cited by 21 publications

(29 citation statements)

References 30 publications

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“…Short-term (30 days or less) alterations in cerebral blood flow (CBF) have previously been reported following UCCAO, with some reports showing prolonged hypoperfusion[4] and others showing an initial hypoperfusion followed by a restoration of flow over two weeks[8]. To clarify the long-term changes in global CBF, CBF was measured in sham and VCI mice 4 months after surgery using dynamic susceptibility contrast-MRI perfusion.…”

Section: Resultsmentioning

confidence: 99%

“…Our data show that CBF is impaired in the ischemic hemisphere for up to 4 months after VCI surgery. UCCAO is known to cause large decreases (50–70%) in CBF in the ischemic hemisphere acutely [8, 4]; however, there has been conflicting evidence in the literature over whether UCCAO leads to permanent reductions in CBF [8, 4]. Prior studies have used non-quantitative measures such as laser Doppler flowmetry [4] or methods that examine CBF in only a small region of the brain, such as confocal imaging through a cranial window [8].…”

Section: Discussionmentioning

confidence: 99%

“…UCCAO is known to cause large decreases (50–70%) in CBF in the ischemic hemisphere acutely [8, 4]; however, there has been conflicting evidence in the literature over whether UCCAO leads to permanent reductions in CBF [8, 4]. Prior studies have used non-quantitative measures such as laser Doppler flowmetry [4] or methods that examine CBF in only a small region of the brain, such as confocal imaging through a cranial window [8]. Using laser Doppler flowmetry, it was shown that although CBF improves over time, it remains decreased by 20–37%, compared to baseline, 28 days after surgery [4, 16].…”

Section: Discussionmentioning

confidence: 99%

“…Studies have shown that relative cerebral perfusion is acutely reduced following UCCAO using non-quantitative methods such as laser Doppler flowmetry [4]. However, using confocal imaging through a cranial window it has also been reported that blood flow is restored over time [8]. Both methods estimate changes in cortical perfusion in only a small region of the brain.…”

Section: Introductionmentioning

confidence: 99%

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Neurobehavioral and Imaging Correlates of Hippocampal Atrophy in a Mouse Model of Vascular Cognitive Impairment

Zuloaga

Zhang

Yeiser

et al. 2015

Transl. Stroke Res.

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Vascular cognitive impairment (VCI) is the second most common cause of dementia. Reduced cerebral blood flow is thought to play a major role in the etiology of VCI. Therefore, chronic cerebral hypoperfusion has been used to model VCI in rodents. The goal of the current study was to determine the histopathological and neuroimaging substrates of neurocognitive impairments in a mouse model of chronic cerebral hypoperfusion induced by unilateral common carotid artery occlusion (UCCAO). Mice were subjected to sham or right UCCAO (VCI) surgeries. Three months later, neurocognitive function was evaluated using the novel object recognition task, Morris water maze, and contextual and cued fear conditioning tests. Next, cerebral perfusion was evaluated with dynamic susceptibility contrast magnetic resonance imaging (MRI) using an ultra-high fieild (11.75 Tesla) animal MRI system. Finally, brain pathology was evaluated using histology and T2 weighted MRI (magnetic resonance imaging). VCI, but not sham, mice had significantly reduced cerebral blood flow in the right vs. left cerebral cortex. VCI mice showed deficits in object recognition. T2 weighted MRI of VCI brains revealed enlargement of lateral ventricles, which corresponded to areas of hippocampal atrophy upon histological analysis. In conclusion, our data demonstrate that the UCCAO model of chronic hypoperfusion induces hippocampal atrophy and ventricular enlargement, resulting in neurocognitive deficits characteristic of VCI.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Neurobehavioral and Imaging Correlates of Hippocampal Atrophy in a Mouse Model of Vascular Cognitive Impairment

Zuloaga

Zhang

Yeiser

et al. 2015

Transl. Stroke Res.

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“…Estes achados demonstraram o envolvimento dos mediadores inflamatórios no sistema nervoso central e da neurodegeneração no déficit cognitivo após isquemia cerebral aguda. cortex 3,4 . Interestingly, reperfusion may paradoxically exacerbate brain injury, by involvement of neutrophils, glial reaction, cytokine and chemokine production 5,6,7 .…”

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Memory deficit associated with increased brain proinflammatory cytokine levels and neurodegeneration in acute ischemic stroke

Silva

Sousa

Miranda

et al. 2015

Arq. Neuro-Psiquiatr.

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The present study aimed to investigate behavioral changes and neuroinflammatory process following left unilateral common carotid artery occlusion (UCCA O ), a model of cerebral ischemia. Post-ischemic behavioral changes following 15 min UCCA O were recorded 24 hours after reperfusion. The novel object recognition task was used to assess learning and memory. After behavioral test, brains from sham and ischemic mice were removed and processed to evaluate central nervous system pathology by TTC and H&E techniques as well as inflammatory mediators by ELISA. UCCA O promoted long-term memory impairment after reperfusion. Infarct areas were observed in the cerebrum by TTC stain. Moreover, the histopathological analysis revealed cerebral necrotic cavities surrounded by ischemic neurons and hippocampal neurodegeneration. In parallel with memory dysfunction, brain levels of TNF-a, IL-1b and CXCL1 were increased post ischemia compared with sham-operated group. These findings suggest an involvement of central nervous system inflammatory mediators and brain damage in cognitive impairment following unilateral acute ischemia.

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Cerebrovascular Gi Proteins Protect Against Brain Hypoperfusion and Collateral Failure in Cerebral Ischemia

et al. 2022

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Cerebral hypoperfusion and vascular dysfunction are closely related to common risk factors for ischemic stroke such as hypertension, dyslipidemia, diabetes, and smoking. The role of inhibitory G protein-dependent receptor (GiPCR) signaling in regulating cerebrovascular functions remains largely elusive. We examined the importance of GiPCR signaling in cerebral blood flow (CBF) and its stability after sudden interruption using various in vivo high-resolution magnetic resonance imaging techniques. To this end, we induced a functional knockout of GiPCR signaling in the brain vasculature by injection of pertussis toxin (PTX). Our results show that PTX induced global brain hypoperfusion and microvascular collapse. When PTX-pretreated animals underwent transient unilateral occlusion of one common carotid artery, CBF was disrupted in the ipsilateral hemisphere resulting in the collapse of the cortically penetrating microvessels. In addition, pronounced stroke features in the affected brain regions appeared in both MRI and histological examination. Our findings suggest an impact of cerebrovascular GiPCR signaling in the maintenance of CBF, which may be useful for novel pharmacotherapeutic approaches to prevent and treat cerebrovascular dysfunction and stroke.

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Capillary Remodeling and Collateral Growth Without Angiogenesis After Unilateral Common Carotid Artery Occlusion in Mice

Abstract: Our results indicate that capillary remodeling, pial artery dilatation and collateral growth without angiogenesis are sufficient mechanisms to restore normal cerebral blood flow after unilateral CCA occlusion.

Cited by 21 publications

References 30 publications

Neurobehavioral and Imaging Correlates of Hippocampal Atrophy in a Mouse Model of Vascular Cognitive Impairment

Neurobehavioral and Imaging Correlates of Hippocampal Atrophy in a Mouse Model of Vascular Cognitive Impairment

Memory deficit associated with increased brain proinflammatory cytokine levels and neurodegeneration in acute ischemic stroke

Cerebrovascular Gi Proteins Protect Against Brain Hypoperfusion and Collateral Failure in Cerebral Ischemia

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