Human Alzheimer and inflammation biomarkers after anesthesia and surgery.
Human Alzheimer and inflammation biomarkers after anesthesia and surgery.
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DOI：
10.1097/aln.0b013e31822e9306
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发表时间：
2011-10
期刊：
影响因子：
8.8
通讯作者：
Eckenhoff RG
中科院分区：
文献类型：
--
作者：
Tang JX;Baranov D;Hammond M;Shaw LM;Eckenhoff MF;Eckenhoff RG
术后认知障碍的患病率，加上越来越多的体外，细胞和动物的证据表明麻醉对神经退行性变的影响，需要进一步研究手术护理和阿尔茨海默病神经病理学之间的相互作用。在这里，我们研究人类脑脊液（CSF）的生物标志物围手术期。11名接受特发性鼻CSF漏矫正的患者加入了本机构审查委员会批准的研究。术前置入腰椎蛛网膜下腔导管。麻醉方式为全静脉麻醉（丙泊酚/瑞芬太尼）或吸入麻醉（七氟烷），具体取决于供应商的选择。在导管放置后（基础）、手术结束时（0 h）以及6、24和48 h采集CSF样本。使用xMAP Luminex免疫测定（Luminex，Austin，TX）分析CSF。患者：53±6岁; 8名女性; 4名接受静脉麻醉，6名接受七氟烷，1名接受混合麻醉。手术持续6.4 ± 2小时。平均CSF淀粉样蛋白β1-42保持不变，但总tau和磷酸化tau 181 P进行性增加，直至至少48 h。总tau蛋白、磷酸化tau蛋白或淀粉样蛋白β1-42水平在麻醉组之间没有差异。24 h时两组脑脊液白细胞介素-10、S100 B和肿瘤坏死因子α的升高相似，但吸入组白细胞介素-6的升高更明显。这些数据表明神经炎症反应强烈，不仅包括通常的标志物（白细胞介素-6、肿瘤坏死因子α、白细胞介素-10），还包括损伤标志物S100 B和tau。总-tau/淀粉样蛋白-β1-42比率以与阿尔茨海默病一致的模式增加，主要是由于总-tau增加而不是淀粉样蛋白-β1-42减少。CSF白细胞介素-6水平的差异表明麻醉管理可能会影响神经炎症反应。
The prevalence of post-operative cognitive disturbance, coupled with growing in vitro, cell and animal evidence suggesting anesthetic effects on neurodegeneration, calls for further study of the interaction between surgical care and Alzheimer neuropathology. Here, we study human cerebral spinal fluid (CSF) biomarkers perioperatively. Eleven patients undergoing idiopathic nasal CSF leak correction joined this Institutional Review Board approved study. Lumbar subarachnoid catheters were placed prior to the procedure. Anesthesia was total intravenous anesthesia (propofol/remifentanil) or inhalational (sevoflurane), depending on provider choice. CSF samples were taken after catheter placement (base), at procedure end (0h), and then at 6, 24 and 48h. CSF was analyzed using xMAP Luminex immunoassay (Luminex, Austin, TX). Patients: 53±6 yrs old; 8 women; 4 received intravenous anesthesia, 6 sevoflurane, 1 mixed. Procedures lasted 6.4 ± 2h. Mean CSF amyloid-β1-42 remained unchanged, but total-tau and phosphorylated-tau181P increased progressively until at least 48h. Total-tau, phosphorylated-tau or amyloid-β1-42 levels were not different between anesthetic groups. CSF interleukin-10, S100B and tumor necrosis factor alpha were increased similarly in both anesthetic groups at 24h, but interleukin-6 was increased more in the inhalational group. These data indicate a robust neuroinflammatory response, including not only the usual markers (interleukin-6, tumor necrosis factor α, interleukin-10), but also S100B and tau, markers of injury. The total-tau/amyloid-β1-42 ratio increased in a pattern consistent with Alzheimer disease, largely due to an increase in total-tau rather than a decline in amyloid-β1-42. The differences in CSF interleukin-6 levels, suggest that anesthetic management may make a difference in neuroinflammatory response.