脑缺血再灌注时微血管的变化。

G J del Zoppo
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摘要

尽管微血管间室对血管内容积的贡献很大,但其对疾病的重要性往往被低估。围绕脑缺血的事件和最近对血栓性或栓塞性卒中中可能导致脑动脉再灌注的策略的兴趣引起了对微血管在缺血和再灌注中可能发挥的作用的询问。除了少数情况外,人们对脑组织中微血管的组织知之甚少。然而,缺血、炎症损伤和感染过程明显影响脑微血管内皮、循环血液室的细胞成分和止血。确切的机制正在研究中。从脑组织中分离的微血管系统的观察,直接可视化的枕皮质微血管,以及允许研究皮层下微血管的原位制备,增加了我们对这些过程的理解。在局灶性脑缺血和再灌注过程中,内皮细胞反应性、凝血系统激活和粒细胞-内皮细胞相互作用的改变是影响微血管完整性的几个已被记录的事件。氧自由基的产生、选择素和整合素的表达和细胞间粘附、血管收缩反应、内皮通透性改变、凝血系统和血小板活化是目前正在研究的一些微血管过程,它们似乎是在缺血和再灌注过程中触发的。鉴于这些事件,脑微血管对缺血性损伤的反应仍然相对未被探索。
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Microvascular changes during cerebral ischemia and reperfusion.

Although the microvascular compartment contributes significantly to intravascular volume, its importance to disease is often underestimated. Events surrounding cerebral ischemia and recent interest in strategies which may lead to cerebral artery reperfusion in thrombotic or embolic stroke have raised enquiries about the role(s) the microvasculature may play during ischemia and reperfusion. Except in a few instances, little is known about the organization of the microvasculature in cerebral tissue. However, it is apparent that ischemia, inflammatory insults, and infectious processes affect the cerebral microvascular endothelia, cellular elements of the circulating blood compartment, and hemostasis. The precise mechanisms are under study. Observations in isolated microvascular systems from brain tissue, direct visualization of the pial cortical vasculature, and in situ preparations which allow study of the subcortical microvasculature have added to our understanding of these processes. During focal cerebral ischemia and reperfusion alterations of endothelial cell reactivity, coagulation system activation, and granulocyte-endothelial cell interactions are a few of the events affecting microvascular integrity which have been documented. Oxygen free radical generation, selectin and integrin expression and intercellular adhesion, vasomotor responses, endothelial permeability changes, and coagulation system and platelet activation are some of the microvascular processes currently under study which appear to be triggered during ischemia and reperfusion. In view of these events the responses of the cerebral microvasculature to ischemic injury remain relatively unexplored.

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