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The neurovascular unit in the setting of stroke
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| Zeitschriftentitel: | Journal of Internal Medicine |
|---|---|
| Personen und Körperschaften: | |
| In: | Journal of Internal Medicine, 267, 2010, 2, S. 156-171 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
|
| Schlagwörter: |
| author_facet |
Del Zoppo, G. J. Del Zoppo, G. J. |
|---|---|
| author |
Del Zoppo, G. J. |
| spellingShingle |
Del Zoppo, G. J. Journal of Internal Medicine The neurovascular unit in the setting of stroke Internal Medicine |
| author_sort |
del zoppo, g. j. |
| spelling |
Del Zoppo, G. J. 0954-6820 1365-2796 Wiley Internal Medicine http://dx.doi.org/10.1111/j.1365-2796.2009.02199.x <jats:p>del Zoppo GJ (University of Washington, Seattle, WA, USA). The neurovascular unit in the setting of stroke (Review). <jats:italic>J Intern Med</jats:italic> 2010; <jats:bold>267:</jats:bold> 156–171.</jats:p><jats:p><jats:bold>Abstract. </jats:bold> Microvessels and neurons respond rapidly and simultaneously in focal regions of ischaemic injury in such a way as to suggest that the responses could be coordinated. The ability of neurons to modulate cerebral blood flow in regions of activation results from neurovascular coupling. But little is known about the microvessel‐to‐neuron direction of the relationship. The presence and participation of intervening glial cells implies the association of microvessels, glia, and neurons in a ‘neurovascular unit’. The interdependent functions of the cellular and matrix components of this theoretical unit have not been rigorously explored, except under conditions of injury where, for the most part, only single components or tissue samples have been studied. Whereas maintenance or timely re‐establishment of flow reduces tissue and neuron injury in both humans and animal models, protection of neuron function in humans has not prevented the evolution of injury despite the inherent mechanisms of neurovascular coupling. However, occlusion of flow to the brain rapidly identifies regions of neuron‐vascular vulnerability within the vascular territory‐at‐risk. These coalesce to become the mature ischaemic lesion. The failure, so far, of clinical trials of neuron protectant agents to achieve detectable tissue salvage could be explained by the vulnerability (and lack of protection) of essential components of the ‘unit’. This presentation summarizes evidence and thoughts on this topic. These support the need to understand component interactions within the neurovascular unit.</jats:p> The neurovascular unit in the setting of stroke Journal of Internal Medicine |
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The neurovascular unit in the setting of stroke |
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The neurovascular unit in the setting of stroke |
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The neurovascular unit in the setting of stroke |
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the neurovascular unit in the setting of stroke |
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Internal Medicine |
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http://dx.doi.org/10.1111/j.1365-2796.2009.02199.x |
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2010 |
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156-171 |
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<jats:p>del Zoppo GJ (University of Washington, Seattle, WA, USA). The neurovascular unit in the setting of stroke (Review). <jats:italic>J Intern Med</jats:italic> 2010; <jats:bold>267:</jats:bold> 156–171.</jats:p><jats:p><jats:bold>Abstract. </jats:bold> Microvessels and neurons respond rapidly and simultaneously in focal regions of ischaemic injury in such a way as to suggest that the responses could be coordinated. The ability of neurons to modulate cerebral blood flow in regions of activation results from neurovascular coupling. But little is known about the microvessel‐to‐neuron direction of the relationship. The presence and participation of intervening glial cells implies the association of microvessels, glia, and neurons in a ‘neurovascular unit’. The interdependent functions of the cellular and matrix components of this theoretical unit have not been rigorously explored, except under conditions of injury where, for the most part, only single components or tissue samples have been studied. Whereas maintenance or timely re‐establishment of flow reduces tissue and neuron injury in both humans and animal models, protection of neuron function in humans has not prevented the evolution of injury despite the inherent mechanisms of neurovascular coupling. However, occlusion of flow to the brain rapidly identifies regions of neuron‐vascular vulnerability within the vascular territory‐at‐risk. These coalesce to become the mature ischaemic lesion. The failure, so far, of clinical trials of neuron protectant agents to achieve detectable tissue salvage could be explained by the vulnerability (and lack of protection) of essential components of the ‘unit’. This presentation summarizes evidence and thoughts on this topic. These support the need to understand component interactions within the neurovascular unit.</jats:p> |
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| description | <jats:p>del Zoppo GJ (University of Washington, Seattle, WA, USA). The neurovascular unit in the setting of stroke (Review). <jats:italic>J Intern Med</jats:italic> 2010; <jats:bold>267:</jats:bold> 156–171.</jats:p><jats:p><jats:bold>Abstract. </jats:bold> Microvessels and neurons respond rapidly and simultaneously in focal regions of ischaemic injury in such a way as to suggest that the responses could be coordinated. The ability of neurons to modulate cerebral blood flow in regions of activation results from neurovascular coupling. But little is known about the microvessel‐to‐neuron direction of the relationship. The presence and participation of intervening glial cells implies the association of microvessels, glia, and neurons in a ‘neurovascular unit’. The interdependent functions of the cellular and matrix components of this theoretical unit have not been rigorously explored, except under conditions of injury where, for the most part, only single components or tissue samples have been studied. Whereas maintenance or timely re‐establishment of flow reduces tissue and neuron injury in both humans and animal models, protection of neuron function in humans has not prevented the evolution of injury despite the inherent mechanisms of neurovascular coupling. However, occlusion of flow to the brain rapidly identifies regions of neuron‐vascular vulnerability within the vascular territory‐at‐risk. These coalesce to become the mature ischaemic lesion. The failure, so far, of clinical trials of neuron protectant agents to achieve detectable tissue salvage could be explained by the vulnerability (and lack of protection) of essential components of the ‘unit’. This presentation summarizes evidence and thoughts on this topic. These support the need to understand component interactions within the neurovascular unit.</jats:p> |
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| spelling | Del Zoppo, G. J. 0954-6820 1365-2796 Wiley Internal Medicine http://dx.doi.org/10.1111/j.1365-2796.2009.02199.x <jats:p>del Zoppo GJ (University of Washington, Seattle, WA, USA). The neurovascular unit in the setting of stroke (Review). <jats:italic>J Intern Med</jats:italic> 2010; <jats:bold>267:</jats:bold> 156–171.</jats:p><jats:p><jats:bold>Abstract. </jats:bold> Microvessels and neurons respond rapidly and simultaneously in focal regions of ischaemic injury in such a way as to suggest that the responses could be coordinated. The ability of neurons to modulate cerebral blood flow in regions of activation results from neurovascular coupling. But little is known about the microvessel‐to‐neuron direction of the relationship. The presence and participation of intervening glial cells implies the association of microvessels, glia, and neurons in a ‘neurovascular unit’. The interdependent functions of the cellular and matrix components of this theoretical unit have not been rigorously explored, except under conditions of injury where, for the most part, only single components or tissue samples have been studied. Whereas maintenance or timely re‐establishment of flow reduces tissue and neuron injury in both humans and animal models, protection of neuron function in humans has not prevented the evolution of injury despite the inherent mechanisms of neurovascular coupling. However, occlusion of flow to the brain rapidly identifies regions of neuron‐vascular vulnerability within the vascular territory‐at‐risk. These coalesce to become the mature ischaemic lesion. The failure, so far, of clinical trials of neuron protectant agents to achieve detectable tissue salvage could be explained by the vulnerability (and lack of protection) of essential components of the ‘unit’. This presentation summarizes evidence and thoughts on this topic. These support the need to understand component interactions within the neurovascular unit.</jats:p> The neurovascular unit in the setting of stroke Journal of Internal Medicine |
| spellingShingle | Del Zoppo, G. J., Journal of Internal Medicine, The neurovascular unit in the setting of stroke, Internal Medicine |
| title | The neurovascular unit in the setting of stroke |
| title_full | The neurovascular unit in the setting of stroke |
| title_fullStr | The neurovascular unit in the setting of stroke |
| title_full_unstemmed | The neurovascular unit in the setting of stroke |
| title_short | The neurovascular unit in the setting of stroke |
| title_sort | the neurovascular unit in the setting of stroke |
| title_unstemmed | The neurovascular unit in the setting of stroke |
| topic | Internal Medicine |
| url | http://dx.doi.org/10.1111/j.1365-2796.2009.02199.x |