title: [An experimental study on the role of early postburn massive escharectomy on the prevention of internal organ dysfunction].
abstract: OBJECTIVE
  To explore the role of massive escharectomy at early postburn stage in the prevention of internal organ dysfunction.
  
  
  METHODS
  (1) Ten cases of severely burned patients were randomly divided into early (A) and non-early escharectomy (B) groups in equal number. Venous blood samples were harvested from the patients of the two groups in 1, 3 and 7 postburn days (PBDs), And the samples from 6 healthy volunteers were taken as the control. The serum was separated from the above blood samples and was employed to stimulate cultured HUVECs in vitro. The cell viability and permeability was observed after the stimulation. (2) Seventy Wistar rats inflicted with 30% TBSA III degree scalding were used as an animal model, and were randomized into early (C, n = 30) and non-early escharectomy (D, n = 30) groups, with 5 normal rats as control in each group. Intra-peritoneal fluid infusion was carried out at 1, 3, 6, 12, 24 and 48 postburn hours (PBHs) in rats in both groups. The rats were killed by blood letting at 1 hour after fluid supplementation. The changes in peritoneal macrophage (M Phi) activation state and plasma contents of LPS, IL-8, PLA(2) and MDA were determined at 48 hours after escharectomy in the rats.
  
  
  RESULTS
  The cell viability and permeability of the HUVECs co-cultured with the serum from burn patients in E group was much better preserved than that in B group. On the other hand, the peritoneal M Phi activation and the plasma contents of LPS, IL-8, PLA(2) and MDA in C group were obviously decreased compared with those in D group.
  
  
  CONCLUSIONS
  Early postburn escharectomy to remove denatured burned tissue were proved to be helpful in ameliorating endothelial injury and in inhibiting activation of inflammatory cells. Therefore, early escharectomy was assumed to be beneficial in the prevention of postburn SIRS and MODS.
authors.affiliation: Institute of Burn Research, Southwestern Hospital, The Third Military Medical University. Chongqing 400038, P.R. China.
authors.forename: Jiahan
authors.initials: J
authors.lastname: Wang
authors.forename: Zongcheng
authors.initials: Z
authors.lastname: Yang
mesh_terms: D000328:Adult; D000818:Animals; D002056:Burns / Q000097:blood / Q000150:complications / Q000601:surgery*; D002455:Cell Division; D002460:Cell Line; D002463:Cell Membrane Permeability; D017077:Culture Media, Conditioned / Q000737:chemistry; D015232:Dinoprostone / Q000378:metabolism; D004730:Endothelium, Vascular / Q000166:cytology; D005260:Female; D006801:Humans; D016209:Interleukin-8 / Q000097:blood; D008070:Lipopolysaccharides / Q000097:blood; D017737:Macrophages, Peritoneal / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D009102:Multiple Organ Failure / Q000209:etiology / Q000517:prevention & control*; D009569:Nitric Oxide / Q000378:metabolism; D010741:Phospholipases A / Q000097:blood / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D017077:Culture Media, Conditioned; D016209:Interleukin-8; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D008315:Malondialdehyde; D010741:Phospholipases A; D015232:Dinoprostone