• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

利用循环内皮细胞评估脓毒症相关 ARDS 的内皮损伤。

Evaluation of endothelial damage in sepsis-related ARDS using circulating endothelial cells.

机构信息

Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles (ULB), 808 Route de Lennik, 1070, Brussels, Belgium.

出版信息

Intensive Care Med. 2015 Feb;41(2):231-8. doi: 10.1007/s00134-014-3589-9. Epub 2014 Dec 16.

DOI:10.1007/s00134-014-3589-9
PMID:25510299
Abstract

PURPOSE

Endothelial cell activation and dysfunction are involved in the pathophysiology of ARDS. Circulating endothelial cells (CECs) may be a useful marker of endothelial dysfunction and damage but have been poorly studied in ARDS. We hypothesized that the CEC count may be elevated in patients with sepsis-related ARDS compared to those with sepsis without ARDS.

METHODS

ARDS was defined according to the Berlin consensus definition. The study population included 17 patients with moderate or severe ARDS, 9 with mild ARDS, 13 with sepsis and no ARDS, 13 non-septic patients, and 12 healthy volunteers. Demographic, hemodynamic, and prognostic variables, including PaO(2)/FiO(2) ratio, 28-day survival, blood lactate, APACHE II, and SOFA score, were recorded. CECs were counted in arterial blood samples using the reference CD146 antibody-based immunomagnetic isolation and UEA1-FITC staining method. Measurements were performed 12-24 h after diagnosis of ARDS and repeated daily for 3 days.

RESULTS

The median day-1 CEC count was significantly higher in patients with moderate or severe ARDS than in mild ARDS or septic-control patients [27.2 (18.3-49.4) vs. 17.4 (11-24.5) cells/ml (p < 0.034), and 18.4 (9.1-31) cells/ml (p < 0.035), respectively]. All septic patients (with or without ARDS) had higher day-1 CEC counts than the non-septic patients [19.6 (14.2-30.6) vs. 10.8 (5.7-13.2) cells/ml, p = 0.002].

CONCLUSION

The day-1 CEC count was significantly higher in ARDS patients than in other critically ill patients, and in moderate or severe ARDS patients compared to those with milder disease, making it a potentially useful marker of ARDS severity.

摘要

目的

内皮细胞的激活和功能障碍与 ARDS 的病理生理学有关。循环内皮细胞(CEC)可能是内皮功能障碍和损伤的有用标志物,但在 ARDS 中研究甚少。我们假设,与没有 ARDS 的败血症患者相比,败血症相关 ARDS 患者的 CEC 计数可能升高。

方法

ARDS 根据柏林共识定义进行定义。研究人群包括 17 例中重度 ARDS 患者、9 例轻度 ARDS 患者、13 例败血症且无 ARDS 患者、13 例非败血症患者和 12 例健康志愿者。记录人口统计学、血流动力学和预后变量,包括 PaO(2)/FiO(2) 比值、28 天生存率、血乳酸、APACHE II 和 SOFA 评分。使用参考 CD146 抗体免疫磁分离和 UEA1-FITC 染色法在动脉血样中计数 CEC。在 ARDS 诊断后 12-24 小时进行测量,并在接下来的 3 天内每天重复测量。

结果

中重度 ARDS 患者的第 1 天 CEC 计数中位数明显高于轻度 ARDS 或败血症对照组患者[27.2(18.3-49.4)比 17.4(11-24.5)细胞/ml(p<0.034)和 18.4(9.1-31)细胞/ml(p<0.035)]。所有败血症患者(有或没有 ARDS)的第 1 天 CEC 计数均高于非败血症患者[19.6(14.2-30.6)比 10.8(5.7-13.2)细胞/ml,p=0.002]。

结论

第 1 天的 CEC 计数在 ARDS 患者中明显高于其他危重病患者,在中重度 ARDS 患者中明显高于轻度疾病患者,使其成为 ARDS 严重程度的一个潜在有用标志物。

相似文献

1
Evaluation of endothelial damage in sepsis-related ARDS using circulating endothelial cells.利用循环内皮细胞评估脓毒症相关 ARDS 的内皮损伤。
Intensive Care Med. 2015 Feb;41(2):231-8. doi: 10.1007/s00134-014-3589-9. Epub 2014 Dec 16.
2
Clinical significance of circulating endothelial cells in patients with severe sepsis or septic shock.严重脓毒症或感染性休克患者循环内皮细胞的临床意义。
Infect Dis (Lond). 2015 Jun;47(6):393-8. doi: 10.3109/00365548.2014.1001999. Epub 2015 Mar 6.
3
The value of circulating long non-coding RNA maternally expressed gene 3 as a predictor of higher acute respiratory distress syndrome risk and 28-day mortality in sepsis patients.循环长非编码 RNA 母系表达基因 3 作为脓毒症患者发生急性呼吸窘迫综合征风险和 28 天死亡率的预测因子的价值。
J Clin Lab Anal. 2020 Nov;34(11):e23488. doi: 10.1002/jcla.23488. Epub 2020 Aug 26.
4
Clinical characteristics and outcomes of sepsis-related vs non-sepsis-related ARDS.脓毒症相关与非脓毒症相关 ARDS 的临床特征和结局。
Chest. 2010 Sep;138(3):559-67. doi: 10.1378/chest.09-2933. Epub 2010 May 27.
5
Plasma Mitochondrial DNA Levels Are Associated With ARDS in Trauma and Sepsis Patients.创伤和脓毒症患者的血浆线粒体 DNA 水平与 ARDS 相关。
Chest. 2020 Jan;157(1):67-76. doi: 10.1016/j.chest.2019.09.028. Epub 2019 Oct 14.
6
Discriminatory ability and prognostic evaluation of presepsin for sepsis-related acute respiratory distress syndrome.降钙素原对脓毒症相关性急性呼吸窘迫综合征的鉴别能力和预后评估。
Sci Rep. 2020 Jun 4;10(1):9114. doi: 10.1038/s41598-020-66121-7.
7
Circulating endothelial and endothelial progenitor cells in patients with severe sepsis.严重脓毒症患者的循环内皮细胞和内皮祖细胞。
Microvasc Res. 2011 Mar;81(2):216-21. doi: 10.1016/j.mvr.2010.11.011. Epub 2010 Dec 3.
8
Biomarkers of lung epithelial injury and inflammation distinguish severe sepsis patients with acute respiratory distress syndrome.肺上皮损伤和炎症的生物标志物可区分患有急性呼吸窘迫综合征的严重脓毒症患者。
Crit Care. 2013 Oct 24;17(5):R253. doi: 10.1186/cc13080.
9
Vascular endothelial injuries and changes of blood coagulation and fibrinolysis indexes in patients with acute respiratory distress syndrome.急性呼吸窘迫综合征患者血管内皮损伤及凝血和纤溶指标变化
Chin Med Sci J. 2004 Dec;19(4):252-6.
10
Heparin-binding protein (HBP): an early marker of respiratory failure after trauma?肝素结合蛋白 (HBP):创伤后呼吸衰竭的早期标志物?
Acta Anaesthesiol Scand. 2013 May;57(5):580-6. doi: 10.1111/aas.12070. Epub 2013 Jan 16.

引用本文的文献

1
Unphosphorylated STAT1 binds to the BST2 transcription promoter, promoting increased AKBA anchoring on HPMECs to alleviate ARDS.未磷酸化的信号转导和转录激活因子1(STAT1)与二氢青蒿酸(AKBA)转录启动子结合,促进AKBA在人肺微血管内皮细胞(HPMECs)上的锚定增加,以减轻急性呼吸窘迫综合征(ARDS)。
Sci Rep. 2025 Apr 30;15(1):15207. doi: 10.1038/s41598-025-00028-z.
2
Pathophysiological mechanisms of ARDS: a narrative review from molecular to organ-level perspectives.急性呼吸窘迫综合征的病理生理机制:从分子到器官水平视角的叙述性综述
Respir Res. 2025 Feb 13;26(1):54. doi: 10.1186/s12931-025-03137-5.
3
S100A8/A9 neutrophils induce mitochondrial dysfunction and PANoptosis in endothelial cells via mitochondrial complex I deficiency during sepsis.

本文引用的文献

1
Prone positioning in severe acute respiratory distress syndrome.俯卧位通气治疗严重急性呼吸窘迫综合征。
N Engl J Med. 2013 Jun 6;368(23):2159-68. doi: 10.1056/NEJMoa1214103. Epub 2013 May 20.
2
Acute respiratory distress syndrome: the Berlin Definition.急性呼吸窘迫综合征:柏林定义。
JAMA. 2012 Jun 20;307(23):2526-33. doi: 10.1001/jama.2012.5669.
3
Relations among glycemic control, circulating endothelial cells, nitric oxide, and flow mediated dilation in patients with type 2 diabetes mellitus.2型糖尿病患者血糖控制、循环内皮细胞、一氧化氮与血流介导的血管舒张之间的关系。
S100A8/A9 中性粒细胞通过脓毒症期间线粒体复合物 I 缺乏诱导内皮细胞线粒体功能障碍和 PANoptosis。
Cell Death Dis. 2024 Jun 28;15(6):462. doi: 10.1038/s41419-024-06849-6.
4
The impact of the new acute respiratory distress syndrome (ARDS) criteria on Berlin criteria ARDS patients: a multicenter cohort study.新急性呼吸窘迫综合征(ARDS)标准对柏林 ARDS 标准患者的影响:一项多中心队列研究。
BMC Med. 2023 Nov 23;21(1):456. doi: 10.1186/s12916-023-03144-7.
5
Endothelial-Related Biomarkers in Evaluation of Vascular Function During Progression of Sepsis After Severe Trauma: New Potential Diagnostic Tools in Sepsis.严重创伤后脓毒症进展过程中血管功能评估的内皮相关生物标志物:脓毒症新的潜在诊断工具
J Inflamm Res. 2023 Jul 6;16:2773-2782. doi: 10.2147/JIR.S418697. eCollection 2023.
6
Role of PFKFB3-driven glycolysis in sepsis.PFKFB3 驱动的糖酵解在脓毒症中的作用。
Ann Med. 2023 Dec;55(1):1278-1289. doi: 10.1080/07853890.2023.2191217.
7
Are circulating endothelial cells the next target for transcriptome-level pathway analysis in ARDS?循环内皮细胞是否是 ARDS 转录组水平通路分析的下一个靶点?
Am J Physiol Lung Cell Mol Physiol. 2023 Apr 1;324(4):L393-L399. doi: 10.1152/ajplung.00353.2022. Epub 2023 Feb 7.
8
Extracorporeal carbon dioxide removal for acute respiratory failure: a review of potential indications, clinical practice and open research questions.体外二氧化碳去除术治疗急性呼吸衰竭:潜在适应证、临床实践和开放性研究问题的综述。
Intensive Care Med. 2022 Oct;48(10):1308-1321. doi: 10.1007/s00134-022-06796-w. Epub 2022 Aug 9.
9
MicroRNA-363-3p/sphingosine-1-phosphate receptor 1 axis inhibits sepsis-induced acute lung injury via the inactivation of nuclear factor kappa-B ligand signaling.微小 RNA-363-3p/鞘氨醇 1-磷酸受体 1 轴通过抑制核因子 κB 配体信号通路抑制脓毒症诱导的急性肺损伤。
Exp Anim. 2022 Aug 5;71(3):305-315. doi: 10.1538/expanim.21-0160. Epub 2022 Jul 23.
10
Short-term protective effect of octreotide on the lungs of rats with experimentally induced sepsis.奥曲肽对实验性脓毒症大鼠肺的短期保护作用。
Ulus Travma Acil Cerrahi Derg. 2022 Jan;28(1):8-14. doi: 10.14744/tjtes.2020.02589.
Exp Clin Endocrinol Diabetes. 2012 Sep;120(8):460-5. doi: 10.1055/s-0032-1306349. Epub 2012 May 25.
4
Evaluation of vascular lesions using circulating endothelial cells in renal transplant patients.评价肾移植患者循环内皮细胞的血管病变。
Clin Transplant. 2012 Jul-Aug;26(4):E344-50. doi: 10.1111/j.1399-0012.2012.01620.x. Epub 2012 Apr 19.
5
Circulating endothelial progenitor cells inversely associate with organ dysfunction in sepsis.循环内皮祖细胞与脓毒症器官功能障碍呈负相关。
Intensive Care Med. 2012 Mar;38(3):429-36. doi: 10.1007/s00134-012-2480-9. Epub 2012 Feb 14.
6
Autotransplantation of circulating endothelial progenitor cells protects against lipopolysaccharide-induced acute lung injury in rabbit.循环内皮祖细胞自体移植可预防脂多糖诱导的兔急性肺损伤。
Int Immunopharmacol. 2011 Oct;11(10):1584-90. doi: 10.1016/j.intimp.2011.05.019. Epub 2011 May 31.
7
Endothelial dysfunction in hypertension in pregnancy: associations between circulating endothelial cells, circulating progenitor cells and plasma von Willebrand factor.妊娠高血压中的血管内皮功能障碍:循环内皮细胞、循环祖细胞和血浆血管性血友病因子之间的关系。
Clin Res Cardiol. 2011 Jun;100(6):531-7. doi: 10.1007/s00392-010-0277-9. Epub 2011 Jan 9.
8
Circulating endothelial and endothelial progenitor cells in patients with severe sepsis.严重脓毒症患者的循环内皮细胞和内皮祖细胞。
Microvasc Res. 2011 Mar;81(2):216-21. doi: 10.1016/j.mvr.2010.11.011. Epub 2010 Dec 3.
9
Randomised controlled trial and parallel economic evaluation of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR).随机对照试验和常规通气支持与体外膜肺氧合治疗成人严重呼吸衰竭的平行经济学评价(CESAR)。
Health Technol Assess. 2010 Jul;14(35):1-46. doi: 10.3310/hta14350.
10
Distinct patterns of circulating endothelial cells in pulmonary hypertension.肺动脉高压患者循环内皮细胞的特征。
Eur Respir J. 2010 Dec;36(6):1284-93. doi: 10.1183/09031936.00130809. Epub 2010 Apr 22.