title: Effect of erythrocytes on brain water content and haem oxygenase-1 expression in rats with traumatic intracerebral haemorrhage.
abstract: BACKGROUND
  Studies have demonstrated that brain oedema formation following spontaneous intracerebral haemorrhage is associated with substances derived from blood clots or blood components. However, these studies did not completely reveal the role of blood components in brain oedema formation following traumatic intracerebral haemorrhage (TICH). Here, we explore the role of erythrocytes in brain oedema development by studying the effect of erythrocytes on brain water content (BWC) and expression of haem oxygenase-1 (HO-1) in rats with TICH.
  
  
  METHODS
  A total of 120 Sprague-Dawley rats were randomly divided into four experimental treatment groups: traumatic brain injury (TBI), TBI plus whole blood (WB), TBI plus lysed red blood cells (RBCs; LRBC) and TBI plus packed RBCs (PRBC). Following TBI, which was established by applying a free-falling device, WB, LRBC or PRBC were infused with stereotactic guidance into the injured cortex to produce a model of TICH. All rats were killed at 1, 3 or 5 days after TBI or TICH. BWC was measured, and immunohistochemistry for HO-1 was performed.
  
  
  RESULTS
  In the WB, PRBC and TBI groups, BWC at 3 days post-TBI or post-TICH was the greatest. However, BWC in the LRBC group at 1 day was markedly higher than that at 3 and 5 days. Comparisons among the four groups showed that BWC in the LRBC group was the highest at 1 day, and the highest at 3 days in the WB and PRBC groups; there was no significant difference at 5 days. Positive expression of HO-1 in the WB, PRBC and LRBC groups coincided with changes in BWC.
  
  
  CONCLUSIONS
  Our results indicate that erythrocytes play an important role in delayed brain oedema formation (3 days post-injury) following TICH, but have no significant influence on brain oedema at early stages (1 day post-injury), and that the mechanisms of delayed brain oedema involve RBC breakdown products.
authors.affiliation: Department of Neurosurgery, the First Affiliated Hospital, Henan University of Science and Technology, Luoyang, China. sbzmd20569@163.com
authors.forename: Bao-Zhong
authors.initials: BZ
authors.lastname: Shi
authors.forename: Xiao-Feng
authors.initials: XF
authors.lastname: Meng
authors.forename: Jian-Xue
authors.initials: JX
authors.lastname: Yang
authors.forename: Xiao-Wei
authors.initials: XW
authors.lastname: Hao
authors.forename: Tao
authors.initials: T
authors.lastname: Cui
authors.forename: Zhao-Feng
authors.initials: ZF
authors.lastname: Lu
authors.forename: Hong-Ri
authors.initials: HR
authors.lastname: Zhang
authors.forename: Jiang-Chao
authors.initials: JC
authors.lastname: Zhou
authors.forename: Jin-Fang
authors.initials: JF
authors.lastname: Liu
mesh_terms: D000818:Animals; D001834:Body Water / Q000502:physiology*; D001929:Brain Edema / Q000097:blood* / Q000209:etiology; D002536:Cerebral Arteries / Q000293:injuries / Q000503:physiopathology*; D020202:Cerebral Hemorrhage, Traumatic / Q000097:blood* / Q000150:complications; D004195:Disease Models, Animal; D004912:Erythrocytes / Q000502:physiology*; D005260:Female; D051547:Heme Oxygenase-1 / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D051547:Heme Oxygenase-1