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
Hauptverfasser: 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
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container_end_page 3430
container_issue 24
container_start_page 3406
container_title Journal of neurotrauma
container_volume 38
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. 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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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