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首页> 外文期刊>Critical care : >Plasma thioredoxin levels during post-cardiac arrest syndrome: relationship with severity and outcome
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Plasma thioredoxin levels during post-cardiac arrest syndrome: relationship with severity and outcome

机译：心脏骤停综合征后血浆硫氧还蛋白水平：与严重程度和预后的关系

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IntroductionDespite experimental evidence, clinical demonstration of acute state of oxidative stress and inflammation during post-cardiac arrest syndrome is lacking. Plasma level of thioredoxin (TRX), a redox-active protein induced under conditions of oxidative stress and inflammation, is increased in various critical care conditions. We determined plasma TRX concentrations after cardiac arrest and assessed relationships with severity and outcome.MethodsRetrospective study of consecutive patients admitted to a single academic intensive care unit (ICU) for out-of-hospital cardiac arrest (between July 2006 and March 2008). Plasma levels of TRX were measured at admission, day (D) 1, 2 and 3.ResultsOf 176 patients included, median TRX values measured in ICU survivors and non-survivors were, respectively: 22 ng/mL (7.8 to 77) vs. 72.4 (21.9 to 117.9) at admission (P < 0.001); 5.9 (3.5 to 25.5) vs. 23.2 (5.8 to 81.4) at D1 (P = 0.003); 10.8 (3.6 to 50.8) vs. 11.7 (4.5 to 66.4) at D2 (P = 0.22); and 16.7 (5.3 to 68.3) vs. 17 (4.3 to 62.9) at D3 (P = 0.96). Patients dying within 24 hours had significantly (P < 0.001) higher TRX levels (118.6 ng/mL (94.8 to 280)) than those who died after 24 hours or survived (50.8 (13.9 to 95.7) and 22 (7.8 to 77)). The area under the ROC curve to predict early death was 0.84 (0.76 to 0.91).TRX levels on admission were significantly correlated with 'low-flow' duration (P = 0.003), sequential organ failure assessment (SOFA) score (P < 0.001), and blood lactate concentration (P < 0.001), but not with 'no-flow' duration or simplified acute physiology score (SAPS) II score. TRX levels and admission arterial pO2 correlated negatively (r = -0.17, P = 0.03). Finally, cardiac arrest with cardiac etiology exhibited lower levels of TRX than in cases of extra-cardiac cause (46 ng/mL (11 to 104) vs. 68 (42 to 137), P = 0.01).ConclusionsOur data show for the first time that TRX levels were elevated early following cardiac arrest, suggestive of oxidative stress and inflammation occurring with this condition. Highest values were found in the most severe patients. TRX could be a useful tool for further exploration and comprehension of post-cardiac arrest syndrome.
机译：引言尽管有实验证据，但缺乏心脏骤停综合征后急性氧化应激和炎症状态的临床证明。在各种重症监护条件下，血浆中的硫氧还蛋白（TRX）是一种在氧化应激和炎症条件下诱导的氧化还原活性蛋白，其血浆水平会增加。我们确定了心脏骤停后血浆TRX的浓度，并评估了其与严重程度和预后的关系。方法回顾性研究连续住院的院外心脏骤停（2006年7月至2008年3月）的单个学术重症监护病房（ICU）。在入院第（D）1、2和3天时测量血浆TRX水平。结果包括176例患者，在ICU幸存者和非幸存者中测得的TRX中位数分别为：22 ng / mL（7.8至77）vs.入院时72.4（21.9至117.9）（P <0.001）; D1时分别为5.9（3.5至25.5）与23.2（5.8至81.4）（P = 0.003）; D2时为10.8（3.6至50.8）与11.7（4.5至66.4）（P = 0.22）;在D3时分别为16.7（5.3至68.3）和17（4.3至62.9）（P = 0.96）。 24小时内死亡的患者的TRX水平（118.6 ng / mL（94.8至280））显着（P <0.001）高于24小时后死亡或存活的患者（50.8（13.9至95.7）和22（7.8至77）） 。 ROC曲线下预测早期死亡的面积为0.84（0.76至0.91）。入院时TRX水平与``低流量''持续时间（P = 0.003），器官功能衰竭评估（SOFA）评分显着相关（P <0.001 ）和血液中的乳酸浓度（P <0.001），但没有“无血流”持续时间或简化的急性生理学评分（SAPS）II评分。 TRX水平与入院动脉血氧分压负相关（r = -0.17，P = 0.03）。最后，具有心脏病因的心脏骤停患者的TRX水平低于心脏外原因（46 ng / mL（11至104）vs.68（42至137），P = 0.01）。心脏骤停后早期TRX水平升高的时间，提示这种情况下会发生氧化应激和炎症。在最严重的患者中发现最高值。 TRX可能是进一步探索和理解心脏骤停后综合征的有用工具。

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