Skeletal muscle ischemia-reperfusion injury: a review of endothelial cell-leukocyte interactions.
Skeletal muscle ischemia-reperfusion injury: a review of endothelial cell-leukocyte interactions.
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DOI：
10.3109/08941939409018281
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发表时间：
1994-01-01
期刊：
影响因子：
--
通讯作者：
Duran, W N
中科院分区：
文献类型：
--
作者：
Sabido, F;Milazzo, V J;Duran, W N
由于其相关的高发病率和死亡率，缺血再灌注损伤仍然是血管外科医生面临的一个难题。缺血期间组织损伤的基础取决于组织氧和能量底物的消耗。细胞损伤（如所记录的细胞水肿和溶酶体脱粒）在缺血仅 30 分钟后就开始。骨骼肌缺血 4-6 小时后会发生不可逆的细胞变化。急性动脉闭塞后，血流恢复预示着生化事件的发生，形成了所谓的再灌注综合征的基础。这种组织损伤在再灌注期间血流量最大的区域最为严重。内皮-白细胞相互作用在缺血再灌注损伤中发挥重要作用。内皮细胞和白细胞都具有产生分子信号、表达粘附蛋白和产生有毒代谢副产物的生化机制和能力。由于缺血再灌注损伤中的微循环变化与炎症中的微循环变化相似，因此白细胞-内皮相互作用可以解释与缺血再灌注损伤早期阶段相关的许多反应。
Ischemia-reperfusion injury remains a difficult problem facing vascular surgeons because of its associated high morbidity and mortality. The basis for tissue injury during ischemia depends on depletion of tissue oxygen and energy substrates. Cell injury, as documented cellular edema and lysosomal degranulation, begins after only 30 min of ischemia. Irreversible cellular changes occur after 4-6 h of skeletal muscle ischemia. Following acute arterial occlusion, the restoration of blood flow heralds the onset of biochemical events, forming the basis of what is known as the reperfusion syndrome. This tissue injury is maximal in areas with the greatest blood flow during reperfusion. Endothelium-leukocyte interactions play an important role in ischemia-reperfusion injury. Both endothelial and white blood cells have the biochemical machinery and capacity to generate molecular signals, to express adhesion proteins, and to produce toxic metabolic by-products. Since the microcirculatory changes in ischemia-reperfusion injury parallel those seen in inflammation, the leukocyte-endothelial interaction can explain many of the reactions associated with the early phases of ischemia-reperfusion injury.