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A non-invasive method to produce pressure ulcers of varying severity in a spinal cord-injured rat model.
Ahmed, A K; Goodwin, C R; Sarabia-Estrada, R; Lay, F; Ansari, A M; Steenbergen, C; Pang, C; Cohen, R; Born, L J; Matsangos, A E; Ng, C; Marti, G P; Abu-Bonsrah, N; Phillips, N A; Suk, I; Sciubba, D M; Harmon, J W.
Affiliation
  • Ahmed AK; Department of Surgery and Hendrix Burn/Wound Laboratory, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Goodwin CR; Department of Neurosurgery, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Sarabia-Estrada R; Department of Neurosurgery, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Lay F; Department of Surgery and Hendrix Burn/Wound Laboratory, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Ansari AM; Department of Surgery and Hendrix Burn/Wound Laboratory, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Steenbergen C; Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Pang C; Department of Surgery and Hendrix Burn/Wound Laboratory, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Cohen R; Department of Surgery and Hendrix Burn/Wound Laboratory, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Born LJ; Department of Surgery and Hendrix Burn/Wound Laboratory, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Matsangos AE; Department of Surgery and Hendrix Burn/Wound Laboratory, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Ng C; Department of Surgery and Hendrix Burn/Wound Laboratory, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Marti GP; Department of Surgery and Hendrix Burn/Wound Laboratory, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Abu-Bonsrah N; Department of Neurosurgery, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Phillips NA; Department of Neurosurgery, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Suk I; Department of Neurosurgery, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Sciubba DM; Department of Neurosurgery, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  • Harmon JW; Department of Surgery and Hendrix Burn/Wound Laboratory, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Spinal Cord ; 54(12): 1096-1104, 2016 Dec.
Article in En | MEDLINE | ID: mdl-27324319
STUDY DESIGN: Experimental study. OBJECTIVES: The objective of this study was to establish a non-invasive model to produce pressure ulcers of varying severity in animals with spinal cord injury (SCI). SETTING: The study was conducted at the Johns Hopkins Hospital in Baltimore, Maryland, USA. METHODS: A mid-thoracic (T7-T9) left hemisection was performed on Sprague-Dawley rats. At 7 days post SCI, rats received varying degrees of pressure on the left posterior thigh region. Laser Doppler Flowmetry was used to record blood flow. Animals were killed 12 days after SCI. A cardiac puncture was performed for blood chemistry, and full-thickness tissue was harvested for histology. RESULTS: Doppler blood flow after SCI prior to pressure application was 237.808±16.175 PFUs at day 7. Following pressure application, there was a statistically significant decrease in blood flow in all pressure-applied groups in comparison with controls with a mean perfusion of 118.361±18.223 (P<0.001). White blood cell counts and creatine kinase for each group were statistically significant from the control group (P=0.0107 and P=0.0028, respectively). CONCLUSIONS: We have created a novel animal model of pressure ulcer formation in the setting of a SCI. Histological analysis revealed different stages of injury corresponding to the amount of pressure the animals were exposed to with decreased blood flow immediately after the insult along with a subsequent marked increase in blood flow the next day, conducive to an ischemia-reperfusion injury (IRI) and a possible inflammatory response following tissue injury. Following ischemia and hypoxia secondary to microcirculation impairment, free radicals generate lipid peroxidation, leading to ischemic tissue damage. Future studies should be aimed at measuring free radicals during this period of increased blood flow, following tissue ischemia.
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Full text: 1 Database: MEDLINE Main subject: Spinal Cord Injuries / Pressure Ulcer / Disease Models, Animal Limits: Animals Language: En Journal: Spinal Cord Journal subject: NEUROLOGIA Year: 2016 Type: Article Affiliation country: United States
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Full text: 1 Database: MEDLINE Main subject: Spinal Cord Injuries / Pressure Ulcer / Disease Models, Animal Limits: Animals Language: En Journal: Spinal Cord Journal subject: NEUROLOGIA Year: 2016 Type: Article Affiliation country: United States