术中氧化损伤与心脏手术患者术后谵妄
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Intraoperative Oxidative Damage and Delirium after Cardiac Surgery
背景与目的
目前，对于术后瞻望的发生机制仍知之甚少，限制了有效治疗的进步。本研究旨在验证一个假说，即术中氧化损伤与瞻望和神经元损伤有关，血脑屏障的破坏可改变这些联系。
方 法
在一项预先指定的队列研究中，400名心脏手术患者参加了阿托伐他汀的临床试验，以减少肾脏损伤和瞻望，用气相色谱-质谱法测定血浆中F2-异前列腺素和异呋喃浓度以量化氧化损伤，用泛素羧基端水解酶L1量化神经元损伤，用酶联免疫吸附试验测定S100钙结合蛋白B量化手术前、术中和术后血脑屏障破坏程度。每天使用意识模糊评估法对重症监护病房的以上患者进行两次评估，以诊断瞻望。我们测量了术中F2-异前列腺素和异呋喃、瞻望(主要指标)和术后泛素羧基端水解酶L1(次要指标)之间的独立相关性，并评估了S100钙结合蛋白B是否改变了这些相关性。
结 果
400例患者中有109例(27.3%)出现瞻望，中位数(第10，90百分位数)为1.0(0.5，3.0)天。在整个队列中，血浆泛素羧基端水解酶L1浓度基线为6.3 ng/ml(2.7，14.9)，术后第1天为12.4 ng/ml(7.9，31.2)。F2-异前列腺素和异呋喃在整个手术过程中增加了，术中F2-异前列腺素和异呋喃的对数转换和与术后瞻望的增加独立相关(比值比，33.70 [95% CI, 1.41 to 9.70]; P = 0.008)，与术后泛素羧基端水解酶L1的增加独立相关（几何均数比值1.42[1.11～1.81]；P=0.005）。在S100钙结合蛋白B升高的患者中，术中F2 -异前列腺素和异呋喃增加与术后泛素羧基端水解酶L1增加之间的相关性增强(P = 0.049)。
结 论
术中氧化损伤与术后瞻望和神经元损伤增加有关，在血脑屏障破坏增加的患者中，氧化损伤与神经元损伤之间的相关性更强。
原始文献摘要
Lopez MG, Hughes CG, DeMatteo A, et al. Intraoperative Oxidative Damage and Delirium after Cardiac Surgery[J]. Anesthesiology, 2019, undefined: undefined.
Background: Mechanisms of postoperative delirium remain poorly understood, limiting development of effective treatments. We tested the hypothesis that intraoperative oxidative damage is associated with delirium and neuronal injury and that disruption of the blood–brain barrier modifies these associations.
Methods: In a prespecified cohort study of 400 cardiac surgery patients enrolled in a clinical trial of atorvastatin to reduce kidney injury and delirium, we measured plasma concentrations of F2-isoprostanes and isofurans using gas chromatography-mass spectrometry to quantify oxidative damage, ubiquitin carboxyl-terminal hydrolase isozyme L1 to quantify neuronal injury, and S100 calcium-binding protein B using enzyme-linked immunosorbent assays to quantify blood–brain barrier disruption before, during, and after surgery. We performed the Confusion Assessment Method for the Intensive Care Unit twice daily to diagnose delirium. We measured the independent associations between intraoperative F2-isoprostanes and isofurans and delirium (primary outcome) and postoperative ubiquitin carboxyl-terminal hydrolase isozyme L1 (secondary outcome), and we assessed if S100 calcium-binding protein B
modified these associations.
Results: Delirium occurred in 109 of 400 (27.3%) patients for a median (10th, 90th percentile) of 1.0 (0.5, 3.0) days. In the total cohort, plasma ubiquitin carboxyl-terminal hydrolase isozyme L1 concentration was 6.3 ng/ml (2.7, 14.9) at baseline and 12.4 ng/ml (7.9, 31.2) on postoperative day 1. F2-isoprostanes and isofurans increased throughout surgery, and the log-transformed sum of intraoperative F2-isoprostanes and isofurans was independently associated with increased odds of postoperative delirium (odds ratio, 3.70 [95% CI, 1.41 to 9.70]; P = 0.008) and with increased postoperative ubiquitin carboxyl-terminal hydrolase isozyme L1 (ratio of geometric means, 1.42 [1.11 to 1.81]; P = 0.005). The association between increased intraoperative F2-isoprostanes and isofurans and increased postoperative ubiquitin carboxyl-terminal hydrolase isozyme L1 was amplified in patients with elevated S100 calcium-binding protein B (P = 0.049).
Conclusions: Intraoperative oxidative damage was associated with increased postoperative delirium and neuronal injury, and the association between oxidative damage and neuronal injury was stronger among patients with increased blood–brain barrier disruption.
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贵州医科大学高鸿教授课题组
翻译：何幼芹 编辑：何幼芹 审校：冯玉蓉 王贵龙
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