title: Severe blunt muscle trauma in rats: only marginal hypoxia in the injured area.
abstract: BACKGROUND
  After severe muscle trauma, hypoxia due to microvascular perfusion failure is generally believed to further increase local injury and to impair healing. However, detailed analysis of hypoxia at the cellular level is missing. Therefore, in the present work, spectroscopic measurements of microvascular blood flow and O2 supply were combined with immunological detection of hypoxic cells to estimate O2 conditions within the injured muscle area.
  
  
  METHODS
  Severe blunt muscle trauma was induced in the right Musculus gastrocnemius of male Wistar rats by a standardized "weight-drop" device. Microvascular blood flow, relative hemoglobin amount, and hemoglobin O2 saturation were determined by laser Doppler and white-light spectroscopy. Hypoxic cells were detected by histologic evaluation of covalent binding of pimonidazole and expression of HIF-1α.
  
  
  RESULTS
  Directly after trauma and until the end of experiment (480 minutes), microvascular blood flow and relative hemoglobin amount were clearly increased. In contrast to blood flow and relative hemoglobin amount, there was no immediate but a delayed increase of microvascular hemoglobin O2 saturation. Pimonidazole immunostaining revealed a hypoxic fraction (percentage area of pimonidazole-labelled muscle cells within the injured area) between 8 to 3%. There was almost no HIF-1α expression detectable in the muscle cells under each condition studied.
  
  
  CONCLUSIONS
  In the early phase (up to 8 hours) after severe blunt muscle trauma, the overall microvascular perfusion of the injured area and thus its O2 supply is clearly increased. This increased O2 supply is obviously sufficient to ensure normoxic (or even hyperoxic) conditions in the vast majority of the cells.
authors.affiliation: University of Duisburg-Essen, Institute of Physiological Chemistry, University Hospital Essen, Essen, Germany.
authors.forename: Kristina
authors.initials: K
authors.lastname: Funk
authors.affiliation: University of Duisburg-Essen, Institute of Physiology, University Hospital Essen, Essen, Germany.
authors.forename: Nina
authors.initials: N
authors.lastname: Scheerer
authors.affiliation: University of Duisburg-Essen, Institute of Physiological Chemistry, University Hospital Essen, Essen, Germany.
authors.forename: Rabea
authors.initials: R
authors.lastname: Verhaegh
authors.affiliation: University of Duisburg-Essen, Institute for Medical Informatics, Biometry and Epidemiology, University Hospital Essen, Essen, Germany.
authors.forename: Carolin
authors.initials: C
authors.lastname: Pütter
authors.affiliation: University of Duisburg-Essen, Institute of Physiology, University Hospital Essen, Essen, Germany.
authors.forename: Joachim
authors.initials: J
authors.lastname: Fandrey
authors.affiliation: University of Duisburg-Essen, Institute of Physiological Chemistry, University Hospital Essen, Essen, Germany.
authors.forename: Herbert
authors.initials: H
authors.lastname: de Groot
mesh_terms: D000818:Animals; D015687:Cell Hypoxia; D004396:Coloring Agents / Q000737:chemistry; D006454:Hemoglobins / Q000378:metabolism; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D008297:Male; D055806:Microvessels / Q000378:metabolism; D018482:Muscle, Skeletal / Q000098:blood supply / Q000293:injuries* / Q000378:metabolism; D009593:Nitroimidazoles / Q000737:chemistry; D010100:Oxygen / Q000378:metabolism; D017208:Rats, Wistar; D014949:Wounds, Nonpenetrating / Q000378:metabolism*
chemical_list: D004396:Coloring Agents; D006454:Hemoglobins; C497444:Hif1a protein, rat; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D009593:Nitroimidazoles; C033815:pimonidazole; D010100:Oxygen