Tumor necrosis factor (TNF) and nitric oxide (NO) mediate the acute cardiovascular effects of endotoxemia.
作者信息
Odeh M
出版信息
Ann Surg. 1997 Mar;225(3):342. doi: 10.1097/00000658-199703000-00020.
Abstract
摘要
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Tumor necrosis factor (TNF) and nitric oxide (NO) mediate the acute cardiovascular effects of endotoxemia.肿瘤坏死因子（TNF）和一氧化氮（NO）介导内毒素血症的急性心血管效应。
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本文引用的文献
1
The role of tumor necrosis factor and nitric oxide in the acute cardiovascular response to endotoxin.肿瘤坏死因子和一氧化氮在内毒素所致急性心血管反应中的作用。
Ann Surg. 1996 Jan;223(1):63-9. doi: 10.1097/00000658-199601000-00009.
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Cardiac depressant effects of oxygen free radicals.氧自由基的心脏抑制作用。
Angiology. 1993 Apr;44(4):257-70. doi: 10.1177/000331979304400401.
3
Tumor necrosis factor-alpha as a myocardial depressant substance.肿瘤坏死因子-α作为一种心肌抑制物质。
Int J Cardiol. 1993 Dec 31;42(3):231-8. doi: 10.1016/0167-5273(93)90053-j.
4
Enhancement of intracellular glutathione protects endothelial cells against oxidant damage.细胞内谷胱甘肽水平的提高可保护内皮细胞免受氧化损伤。
Biochem Biophys Res Commun. 1985 Feb 28;127(1):270-6. doi: 10.1016/s0006-291x(85)80154-6.
5
Tumor necrosis factor provokes superoxide anion generation from neutrophils.
Biochem Biophys Res Commun. 1986 Jun 30;137(3):1094-100. doi: 10.1016/0006-291x(86)90337-2.
6
Enhancement of neutrophil superoxide production by preincubation with recombinant human tumor necrosis factor.通过与重组人肿瘤坏死因子预孵育增强中性粒细胞超氧化物的产生。
J Immunol. 1987 Dec 1;139(11):3783-91.
7
Effect of oxygen free radicals on cardiovascular function at organ and cellular levels.
Am Heart J. 1989 Jun;117(6):1196-202. doi: 10.1016/0002-8703(89)90396-7.
8
Tumor necrosis factor-alpha-mediated decrease in glutathione increases the sensitivity of pulmonary vascular endothelial cells to H2O2.肿瘤坏死因子-α介导的谷胱甘肽减少增加了肺血管内皮细胞对过氧化氢的敏感性。
J Clin Invest. 1992 Mar;89(3):794-802. doi: 10.1172/JCI115658.
9
Interferon-gamma and tumor necrosis factor synergize to induce nitric oxide production and inhibit mitochondrial respiration in vascular smooth muscle cells.干扰素-γ与肿瘤坏死因子协同作用，诱导血管平滑肌细胞产生一氧化氮并抑制其线粒体呼吸。
Circ Res. 1992 Nov;71(5):1268-76. doi: 10.1161/01.res.71.5.1268.
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