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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 ischemia and reperfusion: the pathophysiologic concept as a basis for clinical therapy.
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Cerebral ischemia and reperfusion: the pathophysiologic concept as a basis for clinical therapy.

机译：脑缺血和再灌注：病理生理学概念作为临床治疗的基础。

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The ischemic penumbra has been documented in the laboratory animal as severely hypoperfused, nonfunctional, but still viable brain tissue surrounding the irreversibly damaged ischemic core. Saving the penumbra is the main target of acute stroke therapy, and is the theoretical basis behind the reperfusion concept. In experimental focal ischemia, early reperfusion has been reported to both prevent infarct growth and aggravate edema formation and hemorrhage, depending on the severity and duration of prior ischemia and the efficiency of reperfusion, whereas neuronal damage with or without enlarged infarction also may result from reperfusion (so-called reperfusion injury). Activated neutrophils contribute to vascular reperfusion damage, yet posthypoxic cellular injury occurs in the absence of inflammatory species. Protein synthesis inhibition occurs in neurons during reperfusion after ischemia, underlying the role that these pathways play in prosurvival and proapoptotic processes that may be differentially expressed in vulnerable and resistant regions of the reperfused brain tissue. Ischemia-induced decreases in the mitochondrial capacity for respiratory activity probably contribute to the ongoing impairment of energy metabolism during reperfusion and possibly also the magnitude of changes seen during ischemia. From these experimental data, the concept of single-drug intervention cannot be effective. Further experimental research is needed, especially of the study of biochemical markers of the injury process to establish the role of several drugs.
机译：在实验动物中，缺血性半影​​已被记录为严重不可灌注的缺血性核周围严重灌注不足，无功能但仍可行的脑组织。保留半影是急性中风治疗的主要目标，并且是再灌注概念背后的理论基础。在实验性局灶性局部缺血中，据报道，早期再灌注既可以防止梗塞的生长，又可以加剧水肿的形成和出血，这取决于先前缺血的严重程度和持续时间以及再灌注的效率，而再灌注也可能导致有或没有梗塞的神经元损伤。 （所谓的再灌注损伤）。活化的中性粒细胞导致血管再灌注损伤，但是在缺乏炎症物质的情况下发生了低氧后细胞损伤。蛋白合成抑制在缺血后的再灌注过程中在神经元中发生，其潜在作用是这些途径在存活和促凋亡过程中发挥的作用，这些过程可能在再灌注的脑组织的脆弱和耐药区域中差异表达。缺血引起的线粒体呼吸活动能力下降可能导致再灌注过程中能量代谢的持续损害，也可能导致局部缺血过程中变化的幅度。从这些实验数据来看，单药干预的概念无效。需要进一步的实验研究，尤其是对损伤过程的生化标志物的研究以确立几种药物的作用。

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