Division of Orthopaedics, Department of Surgery, University of Western Ontario, Victoria Hospital, London Health Sciences Center, London, ON, Canada.
J Trauma Acute Care Surg. 2012 May;72(5):1194-201;discussion 1202. doi: 10.1097/TA.0b013e31824d68bd.
Traumatic spinal cord injury (SCI) triggers a systemic inflammatory response (SIR) that contributes to a high incidence of secondary organ complications, particularly after a cervical or high-level thoracic injury. Because liver plays a key role in initiating and propagating the SIR, the aim of this study was to assess the effects that SCI at differing segmental levels has on the intensity of the inflammatory response in the liver.
Using male Wistar rats, clip compression SCI was performed at the 4th thoracic (T4 SCI; high-level SCI) or the 12th thoracic (T12 SCI; low-level SCI) spinal cord segment. Sham-injured rats had a partial laminectomy, but no SCI. Leukocyte recruitment to the liver, hepatic blood flow, and hepatocellular injury/death were assessed using intravital microscopy and histology. Chemokine and cytokine concentrations were assessed in the liver. Outcomes were measured at 1.5 hours, 12 hours, and 24 hours after SCI.
At 12 hours after injury, T4 SCI caused a threefold increase in hepatic leukocyte recruitment compared with T12 SCI (p < 0.05). T4 SCI induced 50% more hepatocyte injury than T12 SCI at 12 hours (p < 0.05). Hepatic blood flow decreased after SCI, but not after sham injury, and stayed decreased only after T4 SCI at 24 hours after injury. The T4 SCI-induced changes were accompanied by increases in the hepatic concentrations of interleukin-1β, leptin, interleukin 10, and cytokine-induced neutrophil chemoattractant-1 at 1.5 hours.
Our findings indicate that traumatic SCI triggers an acute SIR that contributes to hepatocellular injury. SCI-induced remote injury/dysfunction to the liver appears to be transient and is more robust after an upper thoracic SCI compared with a lower thoracic SCI.
外伤性脊髓损伤 (SCI) 会引发全身性炎症反应 (SIR)，这会导致继发性器官并发症的发生率很高，尤其是在颈段或高位胸段损伤后。由于肝脏在引发和传播 SIR 中起着关键作用，因此本研究旨在评估不同节段的 SCI 对肝脏炎症反应强度的影响。
使用雄性 Wistar 大鼠，在第 4 胸椎 (T4 SCI；高位 SCI) 或第 12 胸椎 (T12 SCI；低位 SCI) 脊髓段进行夹压 SCI。假损伤大鼠行部分椎板切除术，但不进行 SCI。使用活体显微镜和组织学评估白细胞向肝脏的募集、肝血流和肝细胞损伤/死亡。评估肝脏中的趋化因子和细胞因子浓度。在 SCI 后 1.5 小时、12 小时和 24 小时测量结果。
损伤后 12 小时，T4 SCI 导致肝脏白细胞募集增加三倍，与 T12 SCI 相比 (p < 0.05)。T4 SCI 在 12 小时引起的肝细胞损伤比 T12 SCI 多 50% (p < 0.05)。SCI 后肝血流减少，但假损伤后不减少，仅在损伤后 24 小时 T4 SCI 后仍减少。T4 SCI 诱导的变化伴随着白细胞介素 1β、瘦素、白细胞介素 10 和细胞因子诱导的中性粒细胞趋化因子-1 的肝浓度在 1.5 小时时增加。
我们的发现表明，外伤性 SCI 会引发急性 SIR，导致肝细胞损伤。SCI 引起的肝脏远处损伤/功能障碍似乎是短暂的，与低位胸段 SCI 相比，高位胸段 SCI 更严重。
