title: Local hemodynamic effects of radiation on the rabbit orbitozygomatic complex with and without cytoprotection.
abstract: BACKGROUND
  The authors have previously demonstrated that radiation-induced craniofacial bone growth inhibition may be ameliorated using the known cytoprotectant amifostine in the infant rabbit orbitozygomatic complex. The authors' hypothesis is that reduction in blood supply plays an important role in inhibiting craniofacial bone growth following radiotherapy and that cytoprotective pretreatment exerts its protective effect by maintaining blood supply.
  
  
  METHODS
  Seven-week-old New Zealand male infant rabbits underwent single-dose orthovoltage irradiation to the right orbitozygomatic complex using established protocols: 0 Gy (sham), 35 Gy, and 35 Gy following pretreatment with amifostine (300 mg/kg administered intravenously). Blood flow to the orbitozygomatic complex, orbitozygomatic complex periosteum, masseter, hemimandible, and overlying skin was measured 1, 14, and 63 days after irradiation, using the modified 15-μm radioactive microsphere technique (n = 18 per group, n = 6 per time point). Orbitozygomatic complex bone specimens were harvested for blood vessel morphometry using safranin O stains at days 1 and 100 after irradiation (n = 20 per group, n = 10 per time point).
  
  
  RESULTS
  Blood flow to the irradiated orbitozygomatic complex was significantly (p < 0.05) greater 1 day after single-dose orthovoltage irradiation compared with nonirradiated controls. This increase was not observed in the amifostine-pretreated animals and was also not seen 14 and 63 days after irradiation. No histomorphometric vessel changes were detected at any time point after irradiation in this study.
  
  
  CONCLUSIONS
  Single-dose orthovoltage irradiation results in a temporary elevation in regional blood flow to the orbitozygomatic complex, returning to control levels within 14 days. Although pretreatment with amifostine attenuates this response, radiation-induced craniofacial bone growth inhibition in this model does not appear to be secondary to hemodynamic alterations.
authors.affiliation: Geneva, Switzerland; Toronto, Ontario, Canada; and Seattle, Wash. From the Pediatric Surgery Clinic, University of Geneva Children's Hospital; the Division of Plastic Surgery, The Hospital for Sick Children, Centre for Craniofacial Care and Research; the Department of Clinical Physics, Ontario Cancer Institute, Princess Margaret Hospital; the Department of Pathology and Laboratory Medicine, Mount Sinai Hospital; The Hospital for Sick Children Research Institute, University of Toronto; and the Department of Surgery, Center for Reconstructive Surgery, University of Washington.
authors.forename: Giorgio C
authors.initials: GC
authors.lastname: La Scala
authors.forename: David A
authors.initials: DA
authors.lastname: O'Donovan
authors.forename: Ivan
authors.initials: I
authors.lastname: Yeung
authors.forename: Iona
authors.initials: I
authors.lastname: Leong
authors.forename: Maria
authors.initials: M
authors.lastname: Mendes
authors.forename: Marianne
authors.initials: M
authors.lastname: Rogers
authors.forename: Peter C
authors.initials: PC
authors.lastname: Neligan
authors.forename: Cho Y
authors.initials: CY
authors.lastname: Pang
authors.forename: Christopher R
authors.initials: CR
authors.lastname: Forrest
mesh_terms: D000818:Animals; D006439:Hemodynamics / Q000528:radiation effects*; D008297:Male; D009915:Orbit; D011817:Rabbits; D015050:Zygoma