Strohmaier W, Werner E R, Wachter H, Redl H, Schlag G
Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria.
Shock. 1996 Oct;6(4):254-8. doi: 10.1097/00024382-199610000-00005.
Bacterial lipopolysaccharides (LPS) induce the activity of guanosine triphosphate (GTP)-cyclohydrolase I (GTP-CHI), the first enzyme in the biosynthesis of tetrahydrobiopterin (H4bip) from GTP in endothelial cells and macrophages. In these and other cells, LPS also acts costimulatory with cytokines, i.e., mainly tumor necrosis factor-alpha (TNF-alpha). H4bip is the cofactor for nitric oxide synthase (NOS). We were interested in comparing the pteridine and nitrate levels in two baboon models: a hyperdynamic sepsis model and a hemorrhagic traumatic shock model. Our results show a similar response of pteridines (H4bip, neopterin) and nitrite/nitrate levels to an immune stimulus. LPS, which peaks rapidly, induces a sustained increase in pteridine levels in septic animals. Since hemorrhagic animals show very little response in terms of cytokine production, it was not possible to measure the induction of neopterin and nitrite/nitrate. This information could aid our understanding of the regulatory mechanisms in various forms of experimental shock.
细菌脂多糖（LPS）可诱导鸟苷三磷酸（GTP）-环水解酶I（GTP-CHI）的活性，该酶是内皮细胞和巨噬细胞中由GTP生物合成四氢生物蝶呤（H4bip）的首个酶。在这些细胞及其他细胞中，LPS还与细胞因子（主要是肿瘤坏死因子-α，TNF-α）起协同刺激作用。H4bip是一氧化氮合酶（NOS）的辅因子。我们感兴趣的是比较两种狒狒模型中的蝶呤和硝酸盐水平：一种是高动力性脓毒症模型，另一种是出血性创伤性休克模型。我们的结果显示，蝶呤（H4bip、新蝶呤）和亚硝酸盐/硝酸盐水平对免疫刺激的反应相似。迅速达到峰值的LPS可诱导脓毒症动物体内蝶呤水平持续升高。由于出血性动物在细胞因子产生方面几乎没有反应，因此无法测定新蝶呤和亚硝酸盐/硝酸盐的诱导情况。这些信息有助于我们理解各种形式实验性休克中的调节机制。
