Gourin C G, Shackford S R
Department of Surgery, College of Medicine, University of Vermont, Burlington, USA.
J Trauma. 1996 Jul;41(1):129-35. doi: 10.1097/00005373-199607000-00021.
Brain injury is associated with the production of oxygen free radicals (OFR) and the accumulation of polymorphonuclear leukocytes (PMN) at the site of injury, both of which may be involved in the evolution of secondary cerebral injury. Intercellular adhesion molecule-1 (ICAM-1) is responsible for adherence of PMNs. We sought to determine whether percussion trauma altered the expression of ICAM-1 and to determine the effect of OFR scavengers on ICAM-1 expression after percussion trauma.
Prospective controlled laboratory research using passage 2 human cerebral microvascular endothelium (HCME).
Cell lysates were collected over 24 hours and analyzed for ICAM-1 by enzyme-linked immunosorbent assay (ELISA) after trauma or incubation with tumor necrosis factor (TNF)-alpha. OFR scavengers were added immediately after trauma with or without previous incubation with TNF-alpha.
Sublethal percussion trauma did not alter ICAM-1 expression by HCME. TNF-alpha upregulated ICAM-1 in percussed and nonpercussed cells with maximal ICAM-1 expression at 24 hours (p < 0.01, ANOVA). However, percussion trauma significantly blunted the response of HCME to TNF-alpha. The addition of OFR scavengers after percussion trauma alone had no effect on ICAM-1 expression at 24 hours, but restored the response of percussed HCME to TNF-alpha.
Percussion trauma alters the response of HCME to cytokine-induced ICAM-1 upregulation, and the normal response is restored by OFR scavengers. This suggests that HCME become dysfunctional after percussion trauma and this dysfunction may be mediated by OFR.
脑损伤与氧自由基（OFR）的产生以及多形核白细胞（PMN）在损伤部位的聚集有关，这两者都可能参与继发性脑损伤的发展。细胞间黏附分子-1（ICAM-1）负责PMN的黏附。我们试图确定撞击创伤是否会改变ICAM-1的表达，并确定OFR清除剂对撞击创伤后ICAM-1表达的影响。
使用第2代人脑血管内皮细胞（HCME）进行前瞻性对照实验室研究。
在创伤后或与肿瘤坏死因子（TNF）-α孵育后24小时收集细胞裂解物，并用酶联免疫吸附测定（ELISA）分析ICAM-1。在创伤后立即添加OFR清除剂，无论是否事先与TNF-α孵育。
亚致死性撞击创伤未改变HCME的ICAM-1表达。TNF-α上调了撞击组和未撞击组细胞中的ICAM-1，在24小时时ICAM-1表达达到最大值（p < 0.01，方差分析）。然而，撞击创伤显著减弱了HCME对TNF-α的反应。单独在撞击创伤后添加OFR清除剂对24小时时的ICAM-1表达没有影响，但恢复了撞击后HCME对TNF-α的反应。
撞击创伤改变了HCME对细胞因子诱导的ICAM-1上调的反应，而OFR清除剂可恢复正常反应。这表明HCME在撞击创伤后功能失调，这种功能失调可能由OFR介导。
