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

Contribution of Brain Processes to Tissue Loss After Spinal Cord Injury: Does a Pain-Induced Rise in Blood Pressure Fuel Hemorrhage?
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DOI:
10.3389/fnsys.2021.733056
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发表时间:
2021
影响因子:
3
通讯作者:
Grau JW
Grau JW
中科院分区:
医学3区
文献类型:
--
作者:
Fauss GNK;Strain MM;Huang YJ;Reynolds JA;Davis JA;Henwood MK;West CR;Grau JW

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脊髓损伤(SCI)后不久的疼痛(伤害性)输入扩大了组织损失(继发性损伤)的面积,并损害长期恢复。有证据表明,伤害性刺激具有这种作用,因为它促进急性出血。中断与大脑的交流会阻止这种效果。目前的研究检查是否喙系统加剧组织损失,因为疼痛输入驱动收缩压(BP)和流量的增加,燃料血液渗透。大鼠接受下胸(T12)脊髓中度挫伤。18小时后在T2切断脊髓,中断与喙突的通讯。对尾巴施加伤害性电刺激(电击)(实验1),或对一只后爪施加刺激性辣椒素(实验2),增加了损伤部位的出血。休克,但不是辣椒素,增加收缩压和尾部血流量在假手术大鼠。切断与大脑的通讯阻断了休克引起的收缩压和尾部血流量的增加。实验3研究了在接受休克的动物中用去甲肾上腺素(NE)人为驱动BP升高的效果。脊髓横断减轻了溶剂处理大鼠的出血。NE治疗使血压和尾部血流量显著增加,但未增加出血程度。结果表明,SCI后的疼痛输入可以参与促进出血和驱动持续心血管输出的喙部过程。然而,血压的升高并不一定或不足以导致出血,而是涉及其他脑依赖性过程。
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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