title: Severity of trauma changes expression of TNF-alpha mRNA in the brain of mice.
abstract: BACKGROUND
  The greater nitrogen loss that occurs with increasing severity of trauma is believed to occur because activation of the hypothalamus-pituitary axis is greater with severe injury. Cytokines in the brain stimulate the hypothalamus-pituitary-adrenal axis. This study was carried out to investigate whether the brain would recognize severity of trauma via TNF-alpha mRNA synthesis in the brain.
  
  
  METHODS
  Male C57BL/6 mice (n = 70, BW: 20-28 g) were randomly assigned into four groups, (1) control (no anesthesia or incision), (2) anesthesia alone, (3) anesthesia plus laparotomy by short incision (short), and (4) anesthesia plus laparotomy by long incision (long). A laparotomy was carried out in the short and long groups by a 1.2-cm vertical incision and by a horizontal plus a vertical incision (2.4 x 2.4 cm), respectively. Exactly either 3 or 24 h after surgery, the animals were decapitated. TNF-alpha mRNA levels in the tissues were determined by semi-quantitative PCR.
  
  
  RESULTS
  Nitrogen and catecholamine excretion were increased in the long wound group compared with the short wound group. Expression of TNF-alpha mRNA in the brain was greater in the long group after surgery than in the control, anesthesia, and short groups (brain, long: 0.150 +/- 0.005; P < 0.01 vs control, anesthesia alone, and short groups), but TNF-alpha levels in the plasma were the same in the short and long groups after surgery.
  
  
  CONCLUSIONS
  Levels of TNF-alpha mRNA in the brain were enhanced according to the length of the wound probably because of greater neural stimuli from the wound site, and this elevation was involved in the greater nitrogen loss.
authors.affiliation: Department of Surgery, Kurume University, Fukuoka, 830-0011, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Kamei
authors.forename: S
authors.initials: S
authors.lastname: Yoshida
authors.forename: K
authors.initials: K
authors.lastname: Yamasaki
authors.forename: T
authors.initials: T
authors.lastname: Tajiri
authors.forename: K
authors.initials: K
authors.lastname: Ozaki
authors.forename: K
authors.initials: K
authors.lastname: Shirouzu
mesh_terms: D000199:Actins / Q000235:genetics; D000818:Animals; D001921:Brain / Q000378:metabolism*; D001930:Brain Injuries / Q000378:metabolism / Q000503:physiopathology*; D007413:Intestinal Mucosa / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010537:Peritoneum / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism*; D015599:Trauma Severity Indices; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000235:genetics*
chemical_list: D000199:Actins; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha