Oredsson S, Qvarfordt P, Plate G
Department of Surgery, Helsingborg Hospital, Lund University, Sweden.
Int Angiol. 1995 Mar;14(1):80-8.
To study the effect of polymorphonuclear leucocytes (PMNLs) on reperfusion injury in rabbit skeletal muscle and to evaluate the role of oxygen-derived free radicals in PMNL-mediated reperfusion injury.
An isolated rabbit limb perfusion model. Amputated hindlimbs were subjected to 4 hours of ischaemia followed by 2 hours of reperfusion with oxygenated Krebs' buffer.
Department of experimental surgery.
14 rabbits.
In group I (n = 8), one limb from each animal was reperfused with PMNL-supplemented buffer while the other limb was reperfused with cell-free buffer (control). In group II (n = 6), SOD and catalase were added to the limb reperfused with PMNL-supplemented buffer while the other limb was reperfused with cell-free buffer without SOD and catalase (control).
PMNL accumulation as myeloperoxidase (MPO) activity, muscle necrosis as uptake of [Tc99]methylenediphosphonate (MDP), and oedema as increase in muscle water content (MWC). Electron microscopy was performed for histological demonstration of reperfusion injury.
Addition of PMNLs increased MPO activity (p < 0.05) and MDP uptake (p < 0.05) but did not affect MWC. SOD and catalase treatment of limbs perfused with PMNLs prevented the increase in MPO activity (p < 0.05) and reduced MDP uptake (p < 0.05) and MWC (p < 0.05). PMNLs aggravated histological changes seen after reperfusion.
Reperfusion injury in skeletal muscle is, at least partially, mediated by PMNLs. Free radical scavengers reduce PMNL-dependent injury and prevent PMNL accumulation suggesting that oxygen-derived free radicals are mediators of PMNL-dependent injury and/or engaged in the interaction between PMNLs and the microvascular endothelium.
研究多形核白细胞（PMNLs）对兔骨骼肌再灌注损伤的影响，并评估氧衍生自由基在PMNL介导的再灌注损伤中的作用。
一个离体兔肢体灌注模型。将截肢后的后肢进行4小时缺血，然后用含氧的 Krebs 缓冲液进行2小时再灌注。
实验外科。
14只兔子。
在第一组（n = 8）中，每只动物的一个肢体用补充了PMNLs的缓冲液进行再灌注，而另一个肢体用无细胞缓冲液进行再灌注（对照）。在第二组（n = 6）中，在补充了PMNLs的缓冲液灌注的肢体中加入超氧化物歧化酶（SOD）和过氧化氢酶，而另一个肢体用不含SOD和过氧化氢酶的无细胞缓冲液进行再灌注（对照）。
以髓过氧化物酶（MPO）活性表示PMNL积聚，以[Tc99]亚甲基二膦酸盐（MDP）摄取表示肌肉坏死，以肌肉含水量（MWC）增加表示水肿。进行电子显微镜检查以组织学显示再灌注损伤。
加入PMNLs可增加MPO活性（p < 0.05）和MDP摄取（p < 0.05），但不影响MWC。用SOD和过氧化氢酶处理灌注了PMNLs的肢体可防止MPO活性增加（p < 0.05），并减少MDP摄取（p < 0.05）和MWC（p < 0.05）。PMNLs加重了再灌注后出现的组织学变化。
骨骼肌的再灌注损伤至少部分是由PMNLs介导 的。自由基清除剂可减少PMNL依赖性损伤并防止PMNL积聚，这表明氧衍生自由基是PMNL依赖性损伤的介质和/或参与了PMNLs与微血管内皮之间的相互作用。
