ArticleSpinal cord2016
A non-invasive method to produce pressure ulcers of varying severity in a spinal cord-injured rat model.
Article in Spinal cord, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Recent advances in the development of hydrogel dressings for the treatment of pressure ulcers/injuries.American journal of translational research · 2025Review
- The rat as an animal model in chronic wound research: An update.Life sciences · 2024Review
- Myoglobin-derived iron causes wound enlargement and impaired regeneration in pressure injuries of muscle.eLife · 2023Article
- Experimental animal modelling for pressure injury: A systematic review.Journal of clinical orthopaedics and trauma · 2021Review
- Noninvasive staging of pressure ulcers using photoacoustic imaging.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2019Article
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
STUDY
designExperimental study.
objectivesThe 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).
settingThe study was conducted at the Johns Hopkins Hospital in Baltimore, Maryland, USA.
methodsA 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.
resultsDoppler 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).
conclusionsWe 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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Registered trials
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