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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Cerebral microvessel responses to focal ischemia.
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Cerebral microvessel responses to focal ischemia.

机译：脑微血管对局灶性缺血的反应。

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摘要

Cerebral microvessels have a unique ultrastructure form, which allows for the close relationship of the endothelium and blood elements to the neurons they serve, via intervening astrocytes. To focal ischemia, the cerebral microvasculature rapidly displays multiple dynamic responses. Immediate events include breakdown of the primary endothelial cell permeability barrier, with transudation of plasma, expression of endothelial cell-leukocyte adhesion receptors, loss of endothelial cell and astrocyte integrin receptors, loss of their matrix ligands, expression of members of several matrix-degrading protease families, and the appearance of receptors associated with angiogenesis and neovascularization. These events occur pari passu with neuron injury. Alterations in the microvessel matrix after the onset of ischemia also suggest links to changes in nonvascular cell viability. Microvascular obstruction within the ischemic territory occurs after occlusion and reperfusion of the feeding arteries ("focal no-reflow" phenomenon). This can result from extrinsic compression and intravascular events, including leukocyte(-platelet) adhesion, platelet-fibrin interactions, and activation of coagulation. All of these events occur in microvessels heterogeneously distributed within the ischemic core. The panorama of acute microvessel responses to focal cerebral ischemia provide opportunities to understand interrelationships between neurons and their microvascular supply and changes that underlie a number of central nervous system neurodegenerative disorders.
机译：脑微血管具有独特的超微结构形式，可通过介入星形胶质细胞使内皮和血液元素与其所服务的神经元紧密联系。对于局灶性缺血，脑微血管迅速显示出多种动态反应。立即发生的事件包括主要内皮细胞通透性障碍的破坏，血浆的渗出，内皮细胞-白细胞粘附受体的表达，内皮细胞和星形胶质整联蛋白受体的缺失，它们的基质配体的缺失，几种降解基质的蛋白酶的成员的表达家族，以及与血管生成和新血管形成相关的受体的出现。这些事件与神经元损伤同等发生。缺血发作后微血管基质的改变也表明与非血管细胞生存力的变化有关。缺血区域内的微血管阻塞发生在进食动脉闭塞和再灌注之后（“局灶性无回流”现象）。这可能是由外在压迫和血管内事件引起的，包括白细胞（-血小板）粘附，血小板-纤维蛋白相互作用和凝血激活。所有这些事件均发生在缺血核心内异质分布的微血管中。急性微血管对局灶性脑缺血反应的全景图提供了了解神经元与其微血管供应和许多中枢神经系统神经退行性疾病基础的变化之间的相互关系的机会。

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