Blunt injury augments interleukin-6 but not tumor necrosis factor in isolated, perfused rat hindlimbs.
Blunt injury augments interleukin-6 but not tumor necrosis factor in isolated, perfused rat hindlimbs.
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在离体、灌注的大鼠后肢中，钝性损伤会增强白细胞介素 6，但不会增强肿瘤坏死因子。
DOI：
10.1097/00005373-199407000-00016
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发表时间：
1994
期刊：
影响因子：
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通讯作者：
Cerra,F
中科院分区：
文献类型：
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作者：
Cipolle,MD;Pasquale,MD;Shearer,J;Caldwell,M;Cerra,F
采用离体灌注大鼠后肢模型，观察钝性组织损伤后的即刻炎症反应。在离体大鼠后肢中建立股骨骨折脱手套模型，用含有白蛋白、洗过的人红细胞（红细胞）、氨基酸和葡萄糖的改良Kreb缓冲液（pH 7.4）在37[度]c下灌注，分别在灌注5、20和80分钟时采集动脉和静脉灌注液。初始实验在灌注空白细胞（wbc）中进行，1组（-inj/-WBC, n= 6）和2组（+ inj/-WBC）。后续实验在含有活化白细胞的灌注液中进行，第3组（-inj/+ WBC, n= 6）和第4组（+ inj/+ WBC, n= 7）。在每次灌注结束时分析后肢肌肉腺苷酸能量电荷（EC）和乳酸与丙酮酸比值（LPR）。该制剂表现出代谢稳定，在80分钟的灌注过程中，氧消耗和乳酸保持稳定，肌肉EC和LPR显示有氧代谢。各组检测肿瘤坏死因子（TNF）、血栓素B2 (TXB2)， 3、4组检测前列腺素F （PGF1 [α]）、白细胞介素6 （IL-6）、髓过氧化物酶（myeloperoxidase）、8-异前列腺素。在wbc后肢初始灌注显示损伤后TNF释放无变化。TXB2水平在灌注过程中升高，与损伤无关。第3组和第4组在80分钟时PGF1 [α]水平升高，而第4组在20分钟时PGF1 [α]水平高于第3组。有趣的是，第4组在80分钟时IL-6水平显著升高，而第3组则没有。脊髓过氧化物酶活性在3组和4.8组的灌注过程中没有明显改变——静脉灌注液中未检测到异前列stane。这些数据表明，IL-6是一种重要的早期介质，直接从灌注良好的损伤组织的内皮中释放。在白细胞存在的情况下，钝性损伤引起这种细胞因子从损伤组织的内皮细胞中早期释放。
An isolated, perfused hindlimb model in rats was used to examine the immediate inflammatory response after blunt tissue injury. A femur-fracture degloving model was used in isolated rat hindlimbs perfused with a modified Kreb's buffer (pH 7.4) containing albumin, washed human red blood cells (RBCs), amino acids, and glucose at 37 [degrees] C. Arterial and venous perfusate was sampled at 5, 20, and 80 minutes of perfusion. Initial experiments were conducted in perfusate void of white blood cells (WBCs), group 1 (-inj/-WBC, n= 6) and group 2 (+ inj/-WBC). Subsequent experiments were conducted in perfusate containing activated WBCs, group 3 (-inj/+ WBC, n= 6) and group 4 (+ inj/+ WBC, n= 7). Hindlimb muscle was analyzed for adenylate energy charge (EC) and lactate-to-pyruvate ratios (LPR) at the end of each perfusion. This preparation appeared metabolically stable in that oxygen consumption and lactate remained stable during the 80-minute perfusion and muscle EC and LPR indicated aerobic metabolism. Tumor necrosis factor (TNF) and thromboxane B2 (TXB2) were measured in all four groups while prostaglandin F (PGF1 [alpha]), IL-6, myeloperoxidase, and 8-isoprostane were measured in groups 3 and 4. Initial perfusions in the-WBC hindlimbs indicated no change in TNF release after injury. The TXB2 level increased during perfusion irrespective of injury. The PGF1 [alpha] was elevated at 80 minutes in both groups 3 and 4, however at 20 minutes PGF1 [alpha] levels were higher in group 4 compared with group 3. Interestingly, the IL-6 level was significantly elevated at 80 minutes in group 4 but not in group 3. Myeloperoxidase activity was not significantly altered during perfusion in either group 3 or 4.8-Isoprostane was not detected in the venous perfusate. These data indicate that IL-6 is an important early mediator released directly from the endothelium of injured tissue that is well perfused. In the presence of WBCs, blunt injury evokes the early release of this cytokine from the endothelium of the injured tissue.