Newman W H, Zhang L M, Leeper-Woodford S K, Castresana M R
Division of Basic Medical Science, Mercer University School of Medicine, Macon, GA., USA.
Crit Care Med. 1996 Feb;24(2):294-7. doi: 10.1097/00003246-199602000-00019.
In septic shock, the principal source of increased plasma concentrations of tumor necrosis factor alpha (TNF) is considered to be the macrophage. Release from the macrophage is stimulated by bacterial lipopolysaccharide (endotoxin). We tested the hypothesis that vascular tissue also responds to endotoxin by releasing TNF.
Prospective repeated measures analysis of timed-release curves.
Anesthesia research laboratory in an academic medical center.
With Institutional Review Board approval and patient consent, segments of internal mammary artery and saphenous vein were obtained during coronary artery bypass surgery.
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Segments of saphenous veins were incubated for 24 hrs in the presence or absence of bacterial lipopolysaccharide. At 0.5, 1, 3, 6, and 24 hrs, medium was assayed for TNF. In other experiments, smooth muscle cells were cultured from saphenous veins, incubated with our without bacterial lipopolysaccharide, and a time-course of TNF release determined. Bacterial lipopolysaccharide (20 micrograms/mL) significantly stimulated release of TNF from venous tissue in a time-dependent manner. At 0.5 hrs, TNF was undetectable in untreated tissue and was 48 +/- 8 U/g wet tissue weight in the presence of bacterial lipopolysaccharide. At 3 hrs, TNF was 43 +/- 27 U/g wet tissue weight in untreated and 388 +/- 185 U/g wet tissue weight in treated (p < .01 vs. control) tissue. Segments of internal mammary artery responded in a similar manner. In smooth muscle cells cultured from saphenous vein and internal mammary artery, bacterial lipopolysaccharide triggered the release of TNF. At 3 hrs, the release of TNF in control cells was 0.2 +/- 0.15 U/mg cell protein and 17 +/- 2 U/mg in the presence of 20 micrograms/mL of bacterial lipopolysaccharide (p < .01 vs. control).
Human blood vessels, both artery and vein, produce TNF potentially from a smooth muscle cell source in response to bacterial lipopolysaccharide.
在感染性休克中，血浆中肿瘤坏死因子α（TNF）浓度升高的主要来源被认为是巨噬细胞。巨噬细胞的释放受到细菌脂多糖（内毒素）的刺激。我们检验了血管组织也会对内毒素作出反应而释放TNF这一假说。
对定时释放曲线进行前瞻性重复测量分析。
一所学术医疗中心的麻醉研究实验室。
经机构审查委员会批准并获得患者同意后，在冠状动脉搭桥手术期间获取乳内动脉和大隐静脉的片段。
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将大隐静脉片段在有或无细菌脂多糖的情况下孵育24小时。在0.5、1、3、6和24小时时，检测培养基中的TNF。在其他实验中，从大隐静脉培养平滑肌细胞，在有或无细菌脂多糖的情况下孵育，并确定TNF释放的时间进程。细菌脂多糖（20微克/毫升）以时间依赖性方式显著刺激静脉组织释放TNF。在0.5小时时，未处理组织中检测不到TNF，在有细菌脂多糖的情况下为48±8U/克湿组织重量。在3小时时，未处理组织中TNF为43±27U/克湿组织重量，处理组（与对照组相比p<0.01）组织中为388±185U/克湿组织重量。乳内动脉片段的反应方式类似。在从大隐静脉和乳内动脉培养的平滑肌细胞中，细菌脂多糖触发了TNF的释放。在3小时时，对照细胞中TNF的释放量为0.2±0.15U/毫克细胞蛋白，在存在20微克/毫升细菌脂多糖的情况下为17±2U/毫克（与对照组相比p<0.01）。
人血管，包括动脉和静脉，在对细菌脂多糖作出反应时可能从平滑肌细胞来源产生TNF。
