title: [Effects of serum of patients with MODS on TF and PAI-1 secretion of human vascular endothelial cells during CRRT].
abstract: OBJECTIVE
  To elucidate the effects of serum of patients with multiple organ dysfunction syndrome (MODS) on tissue factor (TF) and Plasminogen activator inhibitor-1 (PAI-1) secretion of human vascular endothelial cells(HUVEC)during continuous renal replacement therapy (CRRT).
  
  
  METHODS
  Sixteen patients who diagnosed MODS involved were divided into two groups randomly, eight patients treated with CRRT without heparin and the others with heparin for 8 hours. The blood was collected from patients at 0 min, 15 min, 60 min, 120 min and 480 min during CRRT. Serum TNF-alpha, IL-1beta were measured by ELISA.TF and PAI-1 secretion of HUVEC stimulated with serum of patients with MODS undergoing CRRT were detected. TF and PAI-1 expression level were assayed by RT-PCR.
  
  
  RESULTS
  TF and PAI-1 secretion were significantly increased in HUVEC stimulated with serum of patients with MODS, but the levels were decreased after CRRT. There are significant positive correlation between TF or PAI-1 secretion of HUVEC and corresponding serum TNFalpha level in the group without heparin, the coefficient correlation is 0.902 and 0.939(P<0.05)respectively. But there are not significant correlation(P>0.05)in the group with heparin.
  
  
  CONCLUSIONS
  Serum of patients with MODS promote the secretion of TF and PAI-1 in HUVEC.The dysfunction of HUVEC induced by serum of patients with MODS may be related to mediators of inflammation. CRRT can clean up the component which injure HEVEC and improve endothelial cell functions.
authors.affiliation: Department of Nephrology, Third Xiangya Hospital, Central South University, Changsha 410013, China. jwwangdoc@yahoo.com.cn
authors.forename: Jian-wen
authors.initials: JW
authors.lastname: Wang
authors.forename: You-ming
authors.initials: YM
authors.lastname: Peng
authors.forename: Fu-you
authors.initials: FY
authors.lastname: Liu
authors.forename: Hao
authors.initials: H
authors.lastname: Zhang
mesh_terms: D000328:Adult; D000925:Anticoagulants / Q000627:therapeutic use; D002478:Cells, Cultured; D003131:Combined Modality Therapy; D042783:Endothelial Cells / Q000378:metabolism* / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D053583:Interleukin-1beta / Q000097:blood; D008297:Male; D009102:Multiple Organ Failure / Q000097:blood / Q000473:pathology / Q000628:therapy*; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics / Q000378:metabolism*; D017582:Renal Replacement Therapy / Q000379:methods*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D044967:Serum / Q000737:chemistry / Q000502:physiology*; D013925:Thromboplastin / Q000235:genetics / Q000378:metabolism*; D013997:Time Factors; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D000925:Anticoagulants; D053583:Interleukin-1beta; D017395:Plasminogen Activator Inhibitor 1; D014409:Tumor Necrosis Factor-alpha; D006493:Heparin; D013925:Thromboplastin