期刊文献+

细胞因子TNF-α和血管内皮细胞功能标志物与多器官功能衰竭综合征的关系(英文) 被引量:7

Tumor necrosis factor-αand vascular endothelial dysfunction in relation to multiple organ dysfunction syndrome
原文传递
导出
摘要 目的探讨在多器官功能衰竭综合征(MODS)患者中细胞因子TNF-α和血管内皮细胞功能标志物的变化。方法动态观察MODS及非MODS患者一氧化氮(NO)、内皮素(ET-1)、组织纤溶酶原激活物(t-Pa)、纤溶酶原激活物抑制物-1(PAI-1)、循环内皮细胞(CEC)、肿瘤坏死因子(TNF-α)的浓度,同时给予Marshall评分。结果与非MODS组相比,MODS组、死亡组的TNF-α、ET- 1、PAI-1、CEC、Marshall评分显著升高(P<0.05),而NO、t-Pa显著降低(P<0.05)。结论TNF-α作为炎性因子在MODS的进展中起重要作用;在MODS时内皮细胞的损伤表现为ET-1、PAI-1、CEC增加,NO、t-PA减少,Marshall评分对于危重症患者的评估是敏感指标。 Objective To study the changes of vascular endothelial functional status and cytokine TNF-α in patients with multiple organ dysfunction syndrome (MODS). Methods Plasma levels of tissue plasminogen activator (t-Pa), plasminogen activator inhibitor-1 (PAI-1 ), circulating endothelial cell (CEC) and serum levels of endothelin (ET-1 ), tumor necrosis factor- ( (TNF-α), nitric oxide (NO) were determined serially dynamically in patients with MODS and those without MODS (non-MODS). At the same time Marshall scores were evaluated. Results Blood levels of TNF-α, ET-1, PAI-1, CEC, and Marshall scores were significantly higher in MODS and succumbed (those who died) groups than those in non-MODS and survied (those who lived) groups (P 〈0.05), but blood levels of NO and t-Pa were significantly lower ( P 〈 0.05). Conclusion TNF-α played an important role in the progression of MODS. The increase of ET-1, PAI-1, CEC and the decrease of NO and t-Pa indicated endothelial dysfunction in MODS. Marshall scoring system for MODS was a sensitive parameter in evaluating the patients with MODS.
出处 《中华急诊医学杂志》 CAS CSCD 2006年第7期581-584,共4页 Chinese Journal of Emergency Medicine
关键词 肿瘤坏死因子(TNF-α) 多器官功能衰竭综合征 血管内皮细胞功能 细胞因子 标志物 Marshall评分 纤溶酶原激活物抑制物 组织纤溶酶原激活物 危重症患者 MODS Multiple organ dysfunction syndrome (MODS) Endothelial dysfunction Tumor necrosis factor-α (TNF-α) Marshall score
  • 相关文献

参考文献5

二级参考文献40

  • 1程三放,刘红梅,赵小娟,柏玲.SIRS病人凝血障碍的动态变化[J].山西医科大学学报,2004,35(6):598-600. 被引量:8
  • 2王荃,钱素云.生理性抗凝机制在脓毒症中的研究进展[J].国外医学(儿科学分册),2005,32(2):68-71. 被引量:8
  • 3Moncada S, Palmer RM, Higgs EA, et al. Nitric oxide: physiology, pathophysiology, and pharmacology. Pharmacol Rev, 1991, 43: 109-142.
  • 4Hoshida S, Yamashita N, Kuzuya T, et al. Differential effects of longterm renin-angiotensin system blockade on limitation of infarct size in cholesterol-fed rabbits. Atherosclerosis, 2000, 149: 287-294.
  • 5Linz W, Wiemer G, Bemward A, et al. Beneficial effects of bradykinin on myocardial energy metabolism and infarct size. Am J Cardiol, 1997,80 (3A): 118A-123A.
  • 6Koh LK, Bui MN, Hathaway L, et al. Mechanism by which quinapril improves vascular function in coronary artery disease. Am J Cardiol,1999, 83: 327-331.
  • 7Moreau P, d' Uscuo LV, Shaw P, et al. Angiotensin Ⅱ increases tissue endothelin and induces vascular hypertrophy: reversal by ET (A)receptor antagonist. Circulation, 1997, 96: 1593.
  • 8d' Uscuo LV, Shaw P, Barton M, et al. Losartan but not verapamil inhibits angiotensin Ⅱ- induced tissue endothelin-1 increase: role of blood pressure and endothelial function, Hypertension, 1998, 31 : 1035-1310.
  • 9Gram J, Sidelmann J, Jeapersen J. Does low protein concentration of tissue-type plasminogen activator predict a low risk of spontaneous deep vein thrombosis? Thromb Haemost, 1995, 74(2): 718-721.
  • 10Segui R, Estelles A, Mira Y, et al. PAI-1 promotor 4G/5G genptype as an additional risk factor for venous thrombosis in subjects with genetic thrombophilic defects. Br J Haematol, 2000, 111(1): 122-128.

共引文献56

同被引文献43

引证文献7

二级引证文献17

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部