Department of Cardiothoracic Anesthesia and Intensive Care, Sahlgrenska University Hospital, Gothenburg, Sweden.
Ann Thorac Surg. 2012 Aug;94(2):549-55. doi: 10.1016/j.athoracsur.2012.04.044. Epub 2012 Jun 13.
Neurocognitive dysfunction occurs frequently after open-heart surgery. Cerebral microembolization, inflammation, blood-brain barrier (BBB) dysfunction, and impaired cerebral oxygenation are considered among possible etiologies. The relationships between intraoperative microembolic signals and the release of cerebrospinal fluid (CSF) markers of inflammation, neuronal and glial cell injuries, and BBB function were evaluated after cardiac surgery with cardiopulmonary bypass.
Ten patients undergoing aortic valve replacement were included. The CSF was obtained the day before and 24 hours after surgery for assessment of neuronal damage (neuron-specific enolase, total tau, and neurofilament light chain protein), glial cell injury (S-100B, glial fibrillary acidic protein), BBB integrity (CSF to serum albumin ratio) and cytokines (interleukin-6, interleukin-8). Intraoperative extent of microemboli and their occurrence were described using the transcranial Doppler technique.
Intraoperatively, 354±79 microemboli were detected; 81% after release of the aortic cross clamp. The S-100B and glial fibrillary acidic protein increased by 35% (p<0.01) and 25% (p=0.055), respectively. Neuron-specific enolase, total tau, and neurofilament light chain protein, were not significantly affected by the surgery. The CSF albumin increased by 13% (p<0.05) while serum albumin decreased by 27% (p<0.0001). Thus, CSF to serum albumin ratio increased by 61% (p=0.011). There was a 3.5- and 12-fold increase in interleukin-6 (p<0.001) and interleukin-8 (p<0.05), respectively. Microembolic signals did not correlate to changes in CSF glial injury markers, the CSF to serum albumin ratio, or CSF cytokines.
Cardiac surgery with cardiopulmonary bypass causes cerebral inflammation, glial cell injury, and BBB dysfunction without biochemical signs of neuronal damage. These changes are not associated with intraoperative microembolization.
体外循环心脏手术后常发生神经认知功能障碍。脑微栓塞、炎症、血脑屏障（BBB）功能障碍和脑氧合受损被认为是可能的病因。本研究评估了体外循环心脏手术后术中微栓子信号与脑脊液（CSF）炎症标志物、神经元和神经胶质细胞损伤以及 BBB 功能释放之间的关系。
纳入 10 例行主动脉瓣置换术的患者。在手术前一天和手术后 24 小时获取 CSF，以评估神经元损伤（神经元特异性烯醇化酶、总 tau 和神经丝轻链蛋白）、神经胶质细胞损伤（S-100B、胶质纤维酸性蛋白）、BBB 完整性（CSF 与血清白蛋白比值）和细胞因子（白细胞介素-6、白细胞介素-8）。术中使用经颅多普勒技术描述微栓子的程度及其发生情况。
术中检测到 354±79 个微栓子；主动脉阻断释放后 81%。S-100B 和胶质纤维酸性蛋白分别增加 35%（p<0.01）和 25%（p=0.055）。神经元特异性烯醇化酶、总 tau 和神经丝轻链蛋白手术均未受影响。CSF 白蛋白增加 13%（p<0.05），血清白蛋白减少 27%（p<0.0001）。因此，CSF 与血清白蛋白比值增加 61%（p=0.011）。白细胞介素-6（p<0.001）和白细胞介素-8（p<0.05）分别增加了 3.5 倍和 12 倍。微栓子信号与 CSF 神经胶质损伤标志物、CSF 与血清白蛋白比值或 CSF 细胞因子的变化无关。
体外循环心脏手术可引起脑炎症、神经胶质细胞损伤和 BBB 功能障碍，而无神经元损伤的生化迹象。这些变化与术中微栓塞无关。
