The ischemic penumbra: how does tissue injury evolve?
The ischemic penumbra: how does tissue injury evolve?
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DOI：
10.1111/j.1749-6632.2012.06668.x
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发表时间：
2012-01-01
期刊：
影响因子：
--
通讯作者：
Heiss, Wolf-Dieter
中科院分区：
文献类型：
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作者：
Heiss, Wolf-Dieter
如果局部血流能够重建，缺血半暗带有功能恢复的潜力，但如果没有足够的再灌注，就会发生不可逆转的损伤，这取决于缺血的严重程度和持续时间的相互作用。当急性血流低于维持基本内务管理所需的阈值时，核心损伤在几分钟内就确定了。在亚急性期，不可逆转的损伤扩展到半影区：多种电和生物信号由梗塞周围触发，传播抑郁样去极化导致缺氧和乳酸逐步增加。通常在6到8小时内，所有的半影区都会转化为不可逆转的梗塞。在延迟期，继发现象可能会导致额外的组织损伤：紧密连接的破坏会导致血管源性水肿，导致含水量增加和损伤扩大。中性粒细胞和细胞分裂素引起继发性炎症，导致梗塞周围区域和连接纤维束的进一步损害。多模式成像可能能够区分受急性、亚急性或延迟性缺血损伤影响的组织间隔，从而可能为特定阶段的治疗策略提供基础。
An ischemic penumbra has the potential for functional recovery provided that local blood flow can be reestablished, but irreversible damage will develop without sufficient reperfusion, depending on the interaction of severity and duration of ischemia. With acute flows below the threshold required for maintenance of basic housekeeping, injury in the core is established within a few minutes. During the subacute phase, the irreversible damage expands into the penumbra: multiple electrical and biological signals are triggered by periinfarct, spreading depression-like depolarizations leading to hypoxia and stepwise increase in lactate. Usually within 6 to 8 hours, all the penumbra are converted into irreversible infarcts. In a delayed phase, secondary phenomena may cause additional tissue damage: disruption of the tight junctions results in vasogenic edema, leading to increase of water content and damage expansion. Neutrophils and cytokinins cause secondary inflammation, inducing further damage in periinfarct regions and connecting fiber tracts. Multimodal imaging might be able to differentiate among the tissue compartments affected by acute, subacute, or delayed ischemic damage, and thereby might provide the basis for phase-specific treatment strategies.