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Contribution of Brain Processes to Tissue Loss After Spinal Cord Injury: Does a Pain-Induced Rise in Blood Pressure Fuel Hemorrhage?

Pain (nociceptive) input soon after spinal cord injury (SCI) expands the area of tissue loss (secondary injury) and impairs long-term recovery. Evidence suggests that nociceptive stimulation has this effect because it promotes acute hemorrhage. Disrupting communication with the brain blocks this eff...

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Autores principales: Fauss, Gizelle N. K., Strain, Misty M., Huang, Yung-Jen, Reynolds, Joshua A., Davis, Jacob A., Henwood, Melissa K., West, Christopher R., Grau, James W.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8714654/
https://www.ncbi.nlm.nih.gov/pubmed/34975424
http://dx.doi.org/10.3389/fnsys.2021.733056
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author Fauss, Gizelle N. K.
Strain, Misty M.
Huang, Yung-Jen
Reynolds, Joshua A.
Davis, Jacob A.
Henwood, Melissa K.
West, Christopher R.
Grau, James W.
author_facet Fauss, Gizelle N. K.
Strain, Misty M.
Huang, Yung-Jen
Reynolds, Joshua A.
Davis, Jacob A.
Henwood, Melissa K.
West, Christopher R.
Grau, James W.
author_sort Fauss, Gizelle N. K.
collection PubMed
description Pain (nociceptive) input soon after spinal cord injury (SCI) expands the area of tissue loss (secondary injury) and impairs long-term recovery. Evidence suggests that nociceptive stimulation has this effect because it promotes acute hemorrhage. Disrupting communication with the brain blocks this effect. The current study examined whether rostral systems exacerbate tissue loss because pain input drives an increase in systolic blood pressure (BP) and flow that fuels blood infiltration. Rats received a moderate contusion injury to the lower thoracic (T12) spinal cord. Communication with rostral processes was disrupted by cutting the spinal cord 18 h later at T2. Noxious electrical stimulation (shock) applied to the tail (Experiment 1), or application of the irritant capsaicin to one hind paw (Experiment 2), increased hemorrhage at the site of injury. Shock, but not capsaicin, increased systolic BP and tail blood flow in sham-operated rats. Cutting communication with the brain blocked the shock-induced increase in systolic BP and tail blood flow. Experiment 3 examined the effect of artificially driving a rise in BP with norepinephrine (NE) in animals that received shock. Spinal transection attenuated hemorrhage in vehicle-treated rats. Treatment with NE drove a robust increase in BP and tail blood flow but did not increase the extent of hemorrhage. The results suggest pain input after SCI can engage rostral processes that fuel hemorrhage and drive sustained cardiovascular output. An increase in BP was not, however, necessary or sufficient to drive hemorrhage, implicating other brain-dependent processes.
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spelling pubmed-87146542021-12-30 Contribution of Brain Processes to Tissue Loss After Spinal Cord Injury: Does a Pain-Induced Rise in Blood Pressure Fuel Hemorrhage? Fauss, Gizelle N. K. Strain, Misty M. Huang, Yung-Jen Reynolds, Joshua A. Davis, Jacob A. Henwood, Melissa K. West, Christopher R. Grau, James W. Front Syst Neurosci Neuroscience Pain (nociceptive) input soon after spinal cord injury (SCI) expands the area of tissue loss (secondary injury) and impairs long-term recovery. Evidence suggests that nociceptive stimulation has this effect because it promotes acute hemorrhage. Disrupting communication with the brain blocks this effect. The current study examined whether rostral systems exacerbate tissue loss because pain input drives an increase in systolic blood pressure (BP) and flow that fuels blood infiltration. Rats received a moderate contusion injury to the lower thoracic (T12) spinal cord. Communication with rostral processes was disrupted by cutting the spinal cord 18 h later at T2. Noxious electrical stimulation (shock) applied to the tail (Experiment 1), or application of the irritant capsaicin to one hind paw (Experiment 2), increased hemorrhage at the site of injury. Shock, but not capsaicin, increased systolic BP and tail blood flow in sham-operated rats. Cutting communication with the brain blocked the shock-induced increase in systolic BP and tail blood flow. Experiment 3 examined the effect of artificially driving a rise in BP with norepinephrine (NE) in animals that received shock. Spinal transection attenuated hemorrhage in vehicle-treated rats. Treatment with NE drove a robust increase in BP and tail blood flow but did not increase the extent of hemorrhage. The results suggest pain input after SCI can engage rostral processes that fuel hemorrhage and drive sustained cardiovascular output. An increase in BP was not, however, necessary or sufficient to drive hemorrhage, implicating other brain-dependent processes. Frontiers Media S.A. 2021-12-15 /pmc/articles/PMC8714654/ /pubmed/34975424 http://dx.doi.org/10.3389/fnsys.2021.733056 Text en Copyright © 2021 Fauss, Strain, Huang, Reynolds, Davis, Henwood, West and Grau. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Fauss, Gizelle N. K.
Strain, Misty M.
Huang, Yung-Jen
Reynolds, Joshua A.
Davis, Jacob A.
Henwood, Melissa K.
West, Christopher R.
Grau, James W.
Contribution of Brain Processes to Tissue Loss After Spinal Cord Injury: Does a Pain-Induced Rise in Blood Pressure Fuel Hemorrhage?
title Contribution of Brain Processes to Tissue Loss After Spinal Cord Injury: Does a Pain-Induced Rise in Blood Pressure Fuel Hemorrhage?
title_full Contribution of Brain Processes to Tissue Loss After Spinal Cord Injury: Does a Pain-Induced Rise in Blood Pressure Fuel Hemorrhage?
title_fullStr Contribution of Brain Processes to Tissue Loss After Spinal Cord Injury: Does a Pain-Induced Rise in Blood Pressure Fuel Hemorrhage?
title_full_unstemmed Contribution of Brain Processes to Tissue Loss After Spinal Cord Injury: Does a Pain-Induced Rise in Blood Pressure Fuel Hemorrhage?
title_short Contribution of Brain Processes to Tissue Loss After Spinal Cord Injury: Does a Pain-Induced Rise in Blood Pressure Fuel Hemorrhage?
title_sort contribution of brain processes to tissue loss after spinal cord injury: does a pain-induced rise in blood pressure fuel hemorrhage?
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8714654/
https://www.ncbi.nlm.nih.gov/pubmed/34975424
http://dx.doi.org/10.3389/fnsys.2021.733056
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