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Exposure to 100% Oxygen Abolishes the Impairment of Fracture Healing after Thoracic Trauma.

Abstract
In polytrauma patients a thoracic trauma is one of the most critical injuries and an important trigger of post-traumatic inflammation. About 50% of patients with thoracic trauma are additionally affected by bone fractures. The risk for fracture malunion is considerably increased in such patients, the pathomechanisms being poorly understood. Thoracic trauma causes regional alveolar hypoxia and, subsequently, hypoxemia, which in turn triggers local and systemic inflammation. Therefore, we aimed to unravel the role of oxygen in impaired bone regeneration after thoracic trauma. We hypothesized that short-term breathing of 100% oxygen in the early post-traumatic phase ameliorates inflammation and improves bone regeneration. Mice underwent a femur osteotomy alone or combined with blunt chest trauma 100% oxygen was administered immediately after trauma for two separate 3 hour intervals. Arterial blood gas tensions, microcirculatory perfusion and oxygenation were assessed at 3, 9 and 24 hours after injury. Inflammatory cytokines and markers of oxidative/nitrosative stress were measured in plasma, lung and fracture hematoma. Bone healing was assessed on day 7, 14 and 21. Thoracic trauma induced pulmonary and systemic inflammation and impaired bone healing. Short-term exposure to 100% oxygen in the acute post-traumatic phase significantly attenuated systemic and local inflammatory responses and improved fracture healing without provoking toxic side effects, suggesting that hyperoxia could induce anti-inflammatory and pro-regenerative effects after severe injury. These results suggest that breathing of 100% oxygen in the acute post-traumatic phase might reduce the risk of poorly healing fractures in severely injured patients.
AuthorsJulia Kemmler, Ronny Bindl, Oscar McCook, Florian Wagner, Michael Gröger, Katja Wagner, Angelika Scheuerle, Peter Radermacher, Anita Ignatius
JournalPloS one (PLoS One) Vol. 10 Issue 7 Pg. e0131194 ( 2015) ISSN: 1932-6203 [Electronic] United States
PMID26147725 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Cytokines
  • Inflammation Mediators
  • Oxyhemoglobins
  • Carbon Dioxide
  • Oxygen
Topics
  • Acute Lung Injury (etiology, therapy)
  • Animals
  • Bone Regeneration (drug effects)
  • Bony Callus (metabolism)
  • Carbon Dioxide (blood)
  • Cytokines (analysis)
  • DNA Damage
  • Femoral Fractures (etiology, therapy)
  • Fracture Healing (drug effects)
  • Hematoma (metabolism)
  • Hyperoxia (metabolism, physiopathology)
  • Inflammation Mediators (analysis)
  • Lung (chemistry)
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Microcirculation
  • Osteotomy (adverse effects)
  • Oxidative Stress
  • Oxygen (blood)
  • Oxygen Inhalation Therapy
  • Oxyhemoglobins (analysis)
  • Random Allocation
  • Thoracic Injuries (classification, complications, therapy)
  • Weight-Bearing
  • Wounds, Nonpenetrating (classification, complications, therapy)

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