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首页> 外文期刊>Canadian journal of anesthesia: Journal canadien d'anesthesie >Potential biomarkers of tissue hypoxia during acute hemodilutional anemia in cardiac surgery: A prospective study to assess tissue hypoxia as a mechanism of organ injury
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Potential biomarkers of tissue hypoxia during acute hemodilutional anemia in cardiac surgery: A prospective study to assess tissue hypoxia as a mechanism of organ injury

机译：心脏手术中急性血液稀释性贫血期间组织缺氧的潜在生物标志物：评估组织缺氧作为器官损伤机制的前瞻性研究

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Purpose Hemodilutional anemia is associated with acute kidney injury (AKI) and mortality in patients undergoing cardiac surgery by mechanisms that may include tissue hypoxia. Our hypothesis was to assess if changes in the potential hypoxic biomarkers, including methemoglobin and erythropoietin, correlated with a decrease in hemoglobin (Hb) concentration following hemodilution on cardiopulmonary bypass (CPB). Methods Arterial blood samples were taken from patients ( n = 64) undergoing heart surgery and CPB at baseline, during CPB, following CPB, and in the intensive care unit (ICU). Potential hypoxic biomarkers were measured, including methemoglobin, plasma Hb, and erythropoietin. Data were analyzed by repeated measures one-way analysis of variance on ranks and linear regression. Results Hemoglobin levels decreased following CPB and methemoglobin increased in the ICU ( P < 0.001 for both). No correlation was observed between the change in Hb and methemoglobin ( P = 0.23). By contrast, reduced Hb on CPB correlated with increased lactate, reduced pH, and increased erythropoietin levels following CPB ( P ≤ 0.004 for all). Increased plasma Hb ( P < 0.001) also correlated with plasma erythropoietin levels ( P < 0.001). Conclusion These data support the hypothesis that erythropoietin rather than methemoglobin is a potential biomarker of anemia-induced tissue hypoxia. The observed relationships between decreased Hb during CPB and the increase in lactate, reduced pH, and increase in erythropoietin levels suggest that early changes in plasma erythropoietin may be a pragmatic early biomarker of anemia-induced renal hypoxia. Further study is required to determine if anemia-induced increases in erythropoietin may predict AKI in patients undergoing cardiac surgery. Trial registration www.clinicaltrials.gov (NCT01883713). Registered 21 June 2013.
机译：目的血液稀释性贫血与急性肾脏损伤（AKI）和可能包括组织缺氧的机制接受心脏手术的患者死亡率有关。我们的假设是评估潜在的缺氧生物标志物的变化，包括甲基酒蛋白和促红细胞生成素，与血红蛋白（HB）浓度的降低相关，血液渗透旁路（CPB）血液稀释后的血红蛋白（HB）。方法在CPB之后，在CPB期间，在基线上患者（n = 64），在CPB和重症监护室（ICU）中，从患者（n = 64）患者（n = 64）中捕获。测量潜在的缺氧生物标志物，包括甲基酚，血浆HB和促红细胞生成素。通过重复措施分析数据的单向分析，对等级和线性回归的单向分析。结果血红蛋白水平随着CPB和ICU中的增加而增加，ICU增加（两者均为P <0.001）。在Hb和甲状腺蛋白的变化之间没有观察到相关性（P = 0.23）。相比之下，CPB对CPB的降低的Hb与CpB后的增加的乳酸盐，降低pH值和增加的促红细胞生成素水平相关（P≤0.004）。增加的血浆Hb（p <0.001）也与血浆促红细胞生成素水平相关（p <0.001）。结论这些数据支持促红细胞生成素而不是甲基酚的假设是贫血诱导的组织缺氧的潜在生物标志物。 CPB期间降低Hb之间观察到的关系以及乳酸乳酸的增加，降低pH和促红细胞生成素水平的增加表明，血浆促红细胞生成素的早期变化可能是贫血诱导的肾缺氧的务实早期生物标志物。需要进一步研究来确定促血症诱导的促红细胞生成素的增加是否可以预测患有心脏手术的患者的AKI。试用注册www.clinicaltrials.gov（nct01883713）。注册2013年6月21日。

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    Gregory M. T. Hare; Kaho Han; Yevheniy Leshchyshyn; Nikhil Mistry; Tiffanie Kei; Si Yuan Dai; Albert K. Y. Tsui; Razak A. Pirani; Jaideep Honavar; Rakesh P. Patel; Sanjay Yagnik; Shelley L. Welker; Tessa Tam; Alexander Romaschin; Philip W. Connelly; W. Scott Beattie; C. David Mazer;

  • 作者单位

    Department of Anesthesia St. Michael’s Hospital University of Toronto;

    Department of Anesthesia St. Michael’s Hospital University of Toronto;

    Department of Anesthesia St. Michael’s Hospital University of Toronto;

    Department of Anesthesia St. Michael’s Hospital University of Toronto;

    Department of Anesthesia St. Michael’s Hospital University of Toronto;

    Department of Anesthesia St. Michael’s Hospital University of Toronto;

    Department of Anesthesia St. Michael’s Hospital University of Toronto;

    Department of Anesthesia St. Michael’s Hospital University of Toronto;

    Department of Pathology Center for Free Radical Biology University of Alabama at Birmingham;

    Department of Pathology Center for Free Radical Biology University of Alabama at Birmingham;

    Department of Anesthesia St. Michael’s Hospital University of Toronto;

    Department of Perfusion St. Michael’s Hospital University of Toronto;

    Department of Perfusion St. Michael’s Hospital University of Toronto;

    Department of Laboratory Medicine and Pathobiology St. Michael’s Hospital University of Toronto;

    Keenan Research Centre for Biomedical Research Li Ka Shing Knowledge Institute;

    Department of Anesthesia Toronto General Hospital University Health Network University of Toronto;

    Department of Anesthesia St. Michael’s Hospital University of Toronto;

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