Collateral Circulation of the Brain

Hossmann, K.‐A.

doi:10.1007/978-1-4615-3092-3_14

Cited by 10 publications

(10 citation statements)

References 86 publications

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“…Therefore, therapeutic stimulation of arteriogenesis might have important clinical implications for the development of prophylactic and acute treatments of cerebrovascular disease (Love, 2003). In the brain, the circle of Willis is the most efficient collateral system, providing a lowresistance link between the four main supplying arteries (two carotid and two vertebral arteries) (Hossmann, 1993). 3-VO introduced an arteriogenic stimulus by the redistribution of blood flow via the PCA, resulting in a significantly enlarged PCA by 38% within 7 days ( Figure 4E).…”

Section: Discussionmentioning

confidence: 99%

Induction of Cerebral Arteriogenesis Leads to Early-Phase Expression of Protease Inhibitors in Growing Collaterals of the Brain

Hillmeister

Lehmann

Bondke

et al. 2008

J Cereb Blood Flow Metab

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Cerebral arteriogenesis constitutes a promising therapeutic concept for cerebrovascular ischaemia; however, transcriptional profiles important for therapeutic target identification have not yet been investigated. This study aims at a comprehensive characterization of transcriptional and morphologic activation during early-phase collateral vessel growth in a rat model of adaptive cerebral arteriogenesis. Arteriogenesis was induced using a three-vessel occlusion (3-VO) rat model of nonischaemic cerebral hypoperfusion. Collateral tissue from growing posterior cerebral artery (PCA) and posterior communicating artery (Pcom) was selectively isolated avoiding contamination with adjacent tissue. We detected differential gene expression 24 h after 3-VO with 164 genes significantly deregulated. Expression patterns contained gene transcripts predominantly involved in proliferation, inflammation, and migration. By using scanning electron microscopy, morphologic activation of the PCA endothelium was detected. Furthermore, the PCA showed induced proliferation (PCNA staining) and CD68 + macrophage staining 24 h after 3-VO, resulting in a significant increase in diameter within 7 days after 3-VO, confirming the arteriogenic phenotype. Analysis of molecular annotations and networks associated with differentially expressed genes revealed that early-phase cerebral arteriogenesis is characterised by the expression of protease inhibitors. These results were confirmed by quantitative real-time reverse transcription-PCR, and in situ hybridisation localised the expression of tissue inhibitor of metalloproteinase-1 (TIMP-1) and kininogen to collateral arteries, showing that TIMP-1 and kininogen might be molecular markers for early-phase cerebral arteriogenesis.

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Section: Discussionmentioning

confidence: 99%

Induction of Cerebral Arteriogenesis Leads to Early-Phase Expression of Protease Inhibitors in Growing Collaterals of the Brain

Hillmeister

Lehmann

Bondke

et al. 2008

J Cereb Blood Flow Metab

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“…The circle of Willis was discovered by Thomas Willis in the 17th century (53) and connects the major cerebral arteries at the base of the brain. Many more extracranial and intracranial anastomoses have been identified on different levels of the vascular tree, down to capillaries (capillary anastomoses of Pfeifer) (55). However, the parenchymal arteries in the brain are considered to be functional endarteries (55).…”

Section: The Discovery Of the Collateral Circulation And Of Preexistementioning

confidence: 99%

Arteriogenesis The Development and Growth of Collateral Arteries

2003

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In patients with atherosclerotic vascular diseases, collateral vessels bypassing major arterial obstructions have frequently been observed. This may explain why some patients remain without symptoms or signs of ischemia. The term "arteriogenesis" was introduced to differentiate the formation of collateral arteries from angiogenesis, which mainly occurs in the ischemic, collateral flow-dependent tissue. Many observations in various animal models and humans support that the remodeling of preexisting collateral vessels is the mechanism of collateral artery formation. This remodeling process seems to be mainly flow-mediated. It involves endothelial cell activation, basal membrane degradation, leukocyte invasion, proliferation of vascular cells, neointima formation (in most species studied), and changes of the extracellular matrix. The contribution of ischemia to arteriogenesis is still unclear, but arteriogenesis clearly can occur in the absence of any significant ischemia. It is questionable, whether collateral arteries also form de novo in ischemic vascular diseases. A better understanding of the mechanisms of arteriogenesis will be important for the design of more effective strategies for the treatment of patients with ischemic vascular diseases.

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“…These findings directly support the previous proposals. 7,8 The enlarged collaterals provided flow to occluded arterial segments lacking flow after the ligations, indicating recruitment of new flow pathways. Photographs of monkey cortex before and 3 months after small occlusive strokes show increased diameters of arterioles (collaterals) feeding regions around them without tortuosity.…”

Section: Wei Et Al Vascular Changes After Cortical Strokementioning

confidence: 99%

“…2 Reports from stroke models and patients document the proliferation of vascular cells and expression of markers for angiogenesis surrounding infarcts. [3][4][5][6] Few, if any, new large surface vessels have been found in the brain after stroke, 7 although there is evidence of arteriolar collateral enlargement. 8,9 The relationship between angiogenesis and/or vessel growth and function in the brain after focal ischemia has not been characterized.…”

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confidence: 99%

Collateral Growth and Angiogenesis Around Cortical Stroke

Wei

Erinjeri

Rovainen

et al. 2001

Stroke

283

189

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Background and Purpose-We tested the hypothesis that there are significant long-term local vascular changes after ministroke that could form a basis for functional recovery. Methods-A 6-to 8-mm cranial window was opened over the barrel cortex, which was identified by an intrinsic optical signal during mechanical stimulation of the whiskers in anesthetized female Wistar rats. Branches of the middle cerebral artery (MCA) to this region were ligated. Fluorescein isothiocyanate (FITC) transits were recorded by videomicroscopy in each rat just before, immediately after, and 30 days after ligation. Changes in surface vessels and parenchymal perfusion were measured. In similarly prepared rats, angiogenesis was identified by 5-bromo-2-deoxyuridine labeling and immunohistochemistry for the integrin family member ␣ v ␤ 3 . Results-The intrinsic optical signal disappeared immediately after MCA ligations. FITC injection just after ligation demonstrated 3 concentric regions: 1 region of unchanged perfusion, surrounding 1 region of reduced perfusion (the ischemic border) surrounding a central core with little observable perfusion. At 30 days, the following had taken place:(1) diameters and lengths of surface collaterals in the ischemic border had grown significantly, but no new surface vessels were detected, (2) FITC entered occluded MCA segments, (3) arteriocapillary latencies in the ischemic border were shortened compared with latencies just after ligation, and (4) small infarcts were virtually identical to the poorly perfused core. Angiogenesis was confined to the ischemic border. Key Words: cerebral cortex Ⅲ cerebral revascularization Ⅲ microcirclulaton Ⅲ stroke, experimental Ⅲ rats I n the literature on stroke, much attention has been focused on the penumbra. 1 Excitotoxic damage, inflammation, and, ultimately, cell death in the penumbra are possible targets for therapy. 2 Reports from stroke models and patients document the proliferation of vascular cells and expression of markers for angiogenesis surrounding infarcts. [3][4][5][6] Few, if any, new large surface vessels have been found in the brain after stroke, 7 although there is evidence of arteriolar collateral enlargement. 8,9 The relationship between angiogenesis and/or vessel growth and function in the brain after focal ischemia has not been characterized. Conclusions-ArteriolarWithin an hour after creating "ministrokes" in the barrel cortex, there are significant reductions of local cerebral blood flow. 10 The goal of the present study was to evaluate the extent to which perfusion to small regions of ischemia recovers in the functionally identified rat whisker barrel cortex 30 days after ministroke. Specifically, we tested the hypothesis that enlargement and elongation of surface vessels is related to new vessels (angiogenesis) and recovery of flow. If altered surface collaterals can protect ischemic brain from death, they may ultimately support functional neuronal recovery just as angiogenesis may support postischemic myocardial recovery. 11 Normal, ischemic, a...

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Collateral Circulation of the Brain

Cited by 10 publications

References 86 publications

Induction of Cerebral Arteriogenesis Leads to Early-Phase Expression of Protease Inhibitors in Growing Collaterals of the Brain

Induction of Cerebral Arteriogenesis Leads to Early-Phase Expression of Protease Inhibitors in Growing Collaterals of the Brain

Arteriogenesis The Development and Growth of Collateral Arteries

Collateral Growth and Angiogenesis Around Cortical Stroke

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