Department of Medicine, University of Washington, Seattle, WA 98104, USA.
J Intern Med. 2010 Feb;267(2):156-71. doi: 10.1111/j.1365-2796.2009.02199.x.
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.
在缺血性损伤的局部区域，微血管和神经元会迅速且同步地做出反应，这表明它们的反应可能是协调一致的。神经元能够在激活区域调节脑血流，这是由于神经血管耦联的作用。但是，对于微血管到神经元的关系方向，我们知之甚少。中间胶质细胞的存在和参与表明微血管、胶质细胞和神经元在“神经血管单元”中相互关联。这个理论单元的细胞和基质成分的相互依赖的功能除了在损伤条件下，在大多数情况下，只研究了单个成分或组织样本外，尚未得到严格探索。虽然在人和动物模型中，维持或及时重新建立血流可以减少组织和神经元损伤，但尽管存在神经血管耦联的固有机制，神经元功能的保护并不能防止损伤的发展。然而，大脑血流的阻塞可以迅速识别出血管风险区域内神经元-血管的脆弱性区域。这些区域会合并成为成熟的缺血性损伤。到目前为止，神经元保护剂的临床试验未能实现可检测的组织挽救，这可以用“单元”的基本组成部分的脆弱性（和缺乏保护）来解释。本演讲总结了关于这个主题的证据和思考。这些都支持了需要理解神经血管单元内的组件相互作用的必要性。
