Hemorrhage and Locomotor Deficits Induced by Pain Input after Spinal Cord Injury Are Partially Mediated by Changes in Hemodynamics

Strain, Misty M.; Johnston, David T.; Baine, Rachel E; Reynolds, Joshua; Huang, Ya-Ching; Henwood, Melissa K.; Fauss, Gizelle N. K.; Davis, Jacob A.; Miranda, Rajesh C.; West, Christopher R.; Grau, James W.

doi:10.1089/neu.2021.0219

Cited by 6 publications

(20 citation statements)

References 43 publications

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“…Further, this second process cannot reflect a local consequence of nociceptive input, because a transection-induced rise in tail blood flow did not increase hemorrhage in animals that received noxious stimulation. The pattern of results observed here mirror those obtained when animals were pretreated with the alpha-1 adrenergic receptor inverse agonist prazosin, which blocked the pain-induced rise in systolic BP, but augmented blood flow (Strain et al, 2021 ). That treatment too blocked nociception-induced hemorrhage after SCI.…”

Section: Discussionsupporting

confidence: 83%

“…This suggests that nociceptive input can drive hemorrhage and tissue loss independent of these processes. This conclusion is supported by a mediation analysis, which showed that pain input can drive hemorrhage in multiple ways, including a path that is independent of a rise in systolic BP or blood flow (Strain et al, 2021 ). Second, the nociception-induced rise in systolic BP and tail blood flow is brain-dependent and not due to lower level (T2–T6) efferent projections from the spinal cord.…”

Section: Discussionmentioning

confidence: 89%

“…Heart rate and tail blood flow were also assessed. The latter is of interest because past work suggests it can have a dual effect after injury: if the BSCB is intact, an increase in blood flow can lessen cell death by maintaining tissue perfusion (Hamamoto et al, 2007 ; Yuan et al, 2019 ); if the BSCB is compromised, and flow is excessive, it may foster blood infiltration (Strain et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, we did observe some evidence of direct efferent drive in Experiment 2, where we found capsaicin induced a rise in heart rate in both sham-operated and transected rats. Prior analyses, however, have shown that systolic BP and blood flow, not heart rate, predict the extent of nociception-induced hemorrhage after SCI (Strain et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

“…Elsewhere, we performed a mediational analysis that suggests an increase in general blood flow can fuel hemorrhage after SCI (Strain et al, 2021 ). If tail blood flow mirrors both general blood flow and spinal cord blood flow, the heightened tail flow observed after spinal transection should have been associated with amplified hemorrhage.…”

Section: Discussionmentioning

confidence: 99%

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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?

Fauss

Strain

Huang

et al. 2021

Front. Syst. Neurosci.

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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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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 89%