Hemorrhage and Locomotor Deficits Induced by Pain Input after Spinal Cord Injury Are Partially Mediated by Changes in Hemodynamics
Nociceptive input diminishes recovery and increases lesion area after a spinal cord injury (SCI). Recent work has linked these effects to the expansion of hemorrhage at the site of injury. The current article examines whether these adverse effects are linked to a pain-induced rise in blood pressure...
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Veröffentlicht in: | Journal of neurotrauma 2021-12, Vol.38 (24), p.3406-3430 |
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creator | Strain, Misty M Johnston, David T Baine, Rachel E Reynolds, Joshua A Huang, Yung-Jen Henwood, Melissa K Fauss, Gizelle N Davis, Jacob A Miranda, Rajesh C West, Christopher R Grau, James W |
description | Nociceptive input diminishes recovery and increases lesion area after a spinal cord injury (SCI). Recent work has linked these effects to the expansion of hemorrhage at the site of injury. The current article examines whether these adverse effects are linked to a pain-induced rise in blood pressure (BP) and/or flow. Male rats with a low-thoracic SCI were treated with noxious input (electrical stimulation [shock] or capsaicin) soon after injury. Locomotor recovery and BP were assessed throughout. Tissues were collected 3 h, 24 h, or 21 days later. Both electrical stimulation and capsaicin undermined locomotor function and increased the area of hemorrhage. Changes in BP/flow varied depending on type of noxious input, with only shock producing changes in BP. Providing behavioral control over the termination of noxious stimulation attenuated the rise in BP and hemorrhage. Pretreatment with the α-1 adrenergic receptor inverse agonist, prazosin, reduced the stimulation-induced rise in BP and hemorrhage. Prazosin also attenuated the adverse effect that noxious stimulation has on long-term recovery. Administration of the adrenergic agonist, norepinephrine 1 day after injury induced an increase in BP and disrupted locomotor function, but had little effect on hemorrhage. Further, inducing a rise in BP/flow using norepinephrine undermined long-term recovery and increased tissue loss. Mediational analyses suggest that the pain-induced rise in blood flow may foster hemorrhage after SCI. Increased BP appears to act through an independent process to adversely affect locomotor performance, tissue sparing, and long-term recovery. |
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Recent work has linked these effects to the expansion of hemorrhage at the site of injury. The current article examines whether these adverse effects are linked to a pain-induced rise in blood pressure (BP) and/or flow. Male rats with a low-thoracic SCI were treated with noxious input (electrical stimulation [shock] or capsaicin) soon after injury. Locomotor recovery and BP were assessed throughout. Tissues were collected 3 h, 24 h, or 21 days later. Both electrical stimulation and capsaicin undermined locomotor function and increased the area of hemorrhage. Changes in BP/flow varied depending on type of noxious input, with only shock producing changes in BP. Providing behavioral control over the termination of noxious stimulation attenuated the rise in BP and hemorrhage. Pretreatment with the α-1 adrenergic receptor inverse agonist, prazosin, reduced the stimulation-induced rise in BP and hemorrhage. Prazosin also attenuated the adverse effect that noxious stimulation has on long-term recovery. Administration of the adrenergic agonist, norepinephrine 1 day after injury induced an increase in BP and disrupted locomotor function, but had little effect on hemorrhage. Further, inducing a rise in BP/flow using norepinephrine undermined long-term recovery and increased tissue loss. Mediational analyses suggest that the pain-induced rise in blood flow may foster hemorrhage after SCI. Increased BP appears to act through an independent process to adversely affect locomotor performance, tissue sparing, and long-term recovery.</description><identifier>ISSN: 0897-7151</identifier><identifier>EISSN: 1557-9042</identifier><identifier>DOI: 10.1089/neu.2021.0219</identifier><identifier>PMID: 34652956</identifier><language>eng</language><publisher>United States: Mary Ann Liebert, Inc</publisher><subject>Adrenergic receptors ; Animals ; Blood flow ; Blood pressure ; Capsaicin ; Contusions ; Disease Models, Animal ; Electrical stimuli ; Electrodes ; Heart rate ; Hemodynamics ; Hemodynamics - physiology ; Hemorrhage ; Hemorrhage - etiology ; Hypertension ; Inverse agonists ; Laboratory animals ; Locomotion - physiology ; Locomotor activity ; Male ; Norepinephrine ; Original ; Pain ; Pain - etiology ; Pain perception ; Prazosin ; Rats ; Rats, Sprague-Dawley ; Risk Factors ; Side effects ; Spinal cord injuries ; Spinal Cord Injuries - complications ; Spinal Cord Injuries - physiopathology ; Surgery ; Sympathomimetics ; Thorax ; Vertebrae</subject><ispartof>Journal of neurotrauma, 2021-12, Vol.38 (24), p.3406-3430</ispartof><rights>Copyright Mary Ann Liebert, Inc. Dec 2021</rights><rights>Copyright 2021, Mary Ann Liebert, Inc., publishers 2021 Mary Ann Liebert, Inc., publishers</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-b2db6fe16d08adef64b544b7b2a878293689f0649dd241a4b4c05314f04e43753</citedby><cites>FETCH-LOGICAL-c415t-b2db6fe16d08adef64b544b7b2a878293689f0649dd241a4b4c05314f04e43753</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34652956$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Strain, Misty M</creatorcontrib><creatorcontrib>Johnston, David T</creatorcontrib><creatorcontrib>Baine, Rachel E</creatorcontrib><creatorcontrib>Reynolds, Joshua A</creatorcontrib><creatorcontrib>Huang, Yung-Jen</creatorcontrib><creatorcontrib>Henwood, Melissa K</creatorcontrib><creatorcontrib>Fauss, Gizelle N</creatorcontrib><creatorcontrib>Davis, Jacob A</creatorcontrib><creatorcontrib>Miranda, Rajesh C</creatorcontrib><creatorcontrib>West, Christopher R</creatorcontrib><creatorcontrib>Grau, James W</creatorcontrib><title>Hemorrhage and Locomotor Deficits Induced by Pain Input after Spinal Cord Injury Are Partially Mediated by Changes in Hemodynamics</title><title>Journal of neurotrauma</title><addtitle>J Neurotrauma</addtitle><description>Nociceptive input diminishes recovery and increases lesion area after a spinal cord injury (SCI). Recent work has linked these effects to the expansion of hemorrhage at the site of injury. The current article examines whether these adverse effects are linked to a pain-induced rise in blood pressure (BP) and/or flow. Male rats with a low-thoracic SCI were treated with noxious input (electrical stimulation [shock] or capsaicin) soon after injury. Locomotor recovery and BP were assessed throughout. Tissues were collected 3 h, 24 h, or 21 days later. Both electrical stimulation and capsaicin undermined locomotor function and increased the area of hemorrhage. Changes in BP/flow varied depending on type of noxious input, with only shock producing changes in BP. Providing behavioral control over the termination of noxious stimulation attenuated the rise in BP and hemorrhage. Pretreatment with the α-1 adrenergic receptor inverse agonist, prazosin, reduced the stimulation-induced rise in BP and hemorrhage. Prazosin also attenuated the adverse effect that noxious stimulation has on long-term recovery. Administration of the adrenergic agonist, norepinephrine 1 day after injury induced an increase in BP and disrupted locomotor function, but had little effect on hemorrhage. Further, inducing a rise in BP/flow using norepinephrine undermined long-term recovery and increased tissue loss. Mediational analyses suggest that the pain-induced rise in blood flow may foster hemorrhage after SCI. Increased BP appears to act through an independent process to adversely affect locomotor performance, tissue sparing, and long-term recovery.</description><subject>Adrenergic receptors</subject><subject>Animals</subject><subject>Blood flow</subject><subject>Blood pressure</subject><subject>Capsaicin</subject><subject>Contusions</subject><subject>Disease Models, Animal</subject><subject>Electrical stimuli</subject><subject>Electrodes</subject><subject>Heart rate</subject><subject>Hemodynamics</subject><subject>Hemodynamics - physiology</subject><subject>Hemorrhage</subject><subject>Hemorrhage - etiology</subject><subject>Hypertension</subject><subject>Inverse agonists</subject><subject>Laboratory animals</subject><subject>Locomotion - physiology</subject><subject>Locomotor activity</subject><subject>Male</subject><subject>Norepinephrine</subject><subject>Original</subject><subject>Pain</subject><subject>Pain - etiology</subject><subject>Pain perception</subject><subject>Prazosin</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Risk Factors</subject><subject>Side effects</subject><subject>Spinal cord injuries</subject><subject>Spinal Cord Injuries - complications</subject><subject>Spinal Cord Injuries - physiopathology</subject><subject>Surgery</subject><subject>Sympathomimetics</subject><subject>Thorax</subject><subject>Vertebrae</subject><issn>0897-7151</issn><issn>1557-9042</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc2P1CAYh4nRuLOrR6-GxIuXjnyW9mKymVV3kzGaqGdCy9sZJi2MQDfp1b9cJrNu1AMh8D78XuBB6BUla0qa9p2Hec0Io-sy2idoRaVUVUsEe4pWpa4qRSW9QJcpHQihvGbqObrgopaslfUK_bqFKcS4NzvAxlu8DX2YQg4R38DgepcTvvN27sHibsFfjfNlfZwzNkOGiL8dnTcj3oRoy_5hjgu-jlC4mJ0ZxwV_ButMPp_e7I3fQcIl49TVLt5Mrk8v0LPBjAlePsxX6MfHD983t9X2y6e7zfW26gWVueqY7eoBaG1JYywMteikEJ3qmGlUw1peN-1AatFaywQ1ohM9kZyKgQgQXEl-hd6fc49zN4HtwedoRn2MbjJx0cE4_W_Fu73ehXvdKMqlUCXg7UNADD9nSFlPLvUwjsZDmJNmsmENaRVnBX3zH3oIcyxfVai6IJKrlhSqOlN9DClFGB4vQ4k-2dXFrj7Z1Se7hX_99wse6T86-W-BXaGE</recordid><startdate>20211215</startdate><enddate>20211215</enddate><creator>Strain, Misty M</creator><creator>Johnston, David T</creator><creator>Baine, Rachel E</creator><creator>Reynolds, Joshua A</creator><creator>Huang, Yung-Jen</creator><creator>Henwood, Melissa K</creator><creator>Fauss, Gizelle N</creator><creator>Davis, Jacob A</creator><creator>Miranda, Rajesh C</creator><creator>West, Christopher R</creator><creator>Grau, James W</creator><general>Mary Ann Liebert, Inc</general><general>Mary Ann Liebert, Inc., publishers</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20211215</creationdate><title>Hemorrhage and Locomotor Deficits Induced by Pain Input after Spinal Cord Injury Are Partially Mediated by Changes in Hemodynamics</title><author>Strain, Misty M ; 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Recent work has linked these effects to the expansion of hemorrhage at the site of injury. The current article examines whether these adverse effects are linked to a pain-induced rise in blood pressure (BP) and/or flow. Male rats with a low-thoracic SCI were treated with noxious input (electrical stimulation [shock] or capsaicin) soon after injury. Locomotor recovery and BP were assessed throughout. Tissues were collected 3 h, 24 h, or 21 days later. Both electrical stimulation and capsaicin undermined locomotor function and increased the area of hemorrhage. Changes in BP/flow varied depending on type of noxious input, with only shock producing changes in BP. Providing behavioral control over the termination of noxious stimulation attenuated the rise in BP and hemorrhage. Pretreatment with the α-1 adrenergic receptor inverse agonist, prazosin, reduced the stimulation-induced rise in BP and hemorrhage. Prazosin also attenuated the adverse effect that noxious stimulation has on long-term recovery. Administration of the adrenergic agonist, norepinephrine 1 day after injury induced an increase in BP and disrupted locomotor function, but had little effect on hemorrhage. Further, inducing a rise in BP/flow using norepinephrine undermined long-term recovery and increased tissue loss. Mediational analyses suggest that the pain-induced rise in blood flow may foster hemorrhage after SCI. Increased BP appears to act through an independent process to adversely affect locomotor performance, tissue sparing, and long-term recovery.</abstract><cop>United States</cop><pub>Mary Ann Liebert, Inc</pub><pmid>34652956</pmid><doi>10.1089/neu.2021.0219</doi><tpages>25</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adrenergic receptors Animals Blood flow Blood pressure Capsaicin Contusions Disease Models, Animal Electrical stimuli Electrodes Heart rate Hemodynamics Hemodynamics - physiology Hemorrhage Hemorrhage - etiology Hypertension Inverse agonists Laboratory animals Locomotion - physiology Locomotor activity Male Norepinephrine Original Pain Pain - etiology Pain perception Prazosin Rats Rats, Sprague-Dawley Risk Factors Side effects Spinal cord injuries Spinal Cord Injuries - complications Spinal Cord Injuries - physiopathology Surgery Sympathomimetics Thorax Vertebrae |
title | Hemorrhage and Locomotor Deficits Induced by Pain Input after Spinal Cord Injury Are Partially Mediated by Changes in Hemodynamics |
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