A non-invasive method to produce pressure ulcers of varying severity in a spinal cord-injured rat model

A. K. Ahmed, C. R. Goodwin, Rachel Sarabia Estrada, F. Lay, A. M. Ansari, C. Steenbergen, C. Pang, R. Cohen, L. J. Born, A. E. Matsangos, C. Ng, G. P. Marti, N. Abu-Bonsrah, N. A. Phillips, I. Suk, D. M. Sciubba, J. W. Harmon

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1096-1104
Number of pages9
JournalSpinal Cord
Volume54
Issue number12
DOIs
StatePublished - Dec 1 2016
Externally publishedYes

Fingerprint

Pressure Ulcer
Spinal Cord
Spinal Cord Injuries
Pressure
Free Radicals
Ischemia
Baltimore
Laser-Doppler Flowmetry
Wounds and Injuries
Microcirculation
Creatine Kinase
Thigh
Reperfusion Injury
Leukocyte Count
Punctures
Lipid Peroxidation
Sprague Dawley Rats
Histology
Research Design
Thorax

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

Cite this

Ahmed, A. K., Goodwin, C. R., Sarabia Estrada, R., Lay, F., Ansari, A. M., Steenbergen, C., ... Harmon, J. W. (2016). A non-invasive method to produce pressure ulcers of varying severity in a spinal cord-injured rat model. Spinal Cord, 54(12), 1096-1104. https://doi.org/10.1038/sc.2016.61

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, Rachel; 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.

In: Spinal Cord, Vol. 54, No. 12, 01.12.2016, p. 1096-1104.

Research output: Contribution to journalArticle

Ahmed, AK, Goodwin, CR, Sarabia Estrada, R, Lay, F, Ansari, AM, Steenbergen, C, Pang, C, Cohen, R, Born, LJ, Matsangos, AE, Ng, C, Marti, GP, Abu-Bonsrah, N, Phillips, NA, Suk, I, Sciubba, DM & Harmon, JW 2016, 'A non-invasive method to produce pressure ulcers of varying severity in a spinal cord-injured rat model', Spinal Cord, vol. 54, no. 12, pp. 1096-1104. https://doi.org/10.1038/sc.2016.61
Ahmed, A. K. ; Goodwin, C. R. ; Sarabia Estrada, Rachel ; 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. / A non-invasive method to produce pressure ulcers of varying severity in a spinal cord-injured rat model. In: Spinal Cord. 2016 ; Vol. 54, No. 12. pp. 1096-1104.
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abstract = "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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AU - Ahmed, A. K.

AU - Goodwin, C. R.

AU - Sarabia Estrada, Rachel

AU - Lay, F.

AU - Ansari, A. M.

AU - Steenbergen, C.

AU - Pang, C.

AU - Cohen, R.

AU - Born, L. J.

AU - Matsangos, A. E.

AU - Ng, C.

AU - Marti, G. P.

AU - Abu-Bonsrah, N.

AU - Phillips, N. A.

AU - Suk, I.

AU - Sciubba, D. M.

AU - Harmon, J. W.

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N2 - 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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