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心脏停搏后综合征中内皮糖萼的紊乱。

Perturbation of the endothelial glycocalyx in post cardiac arrest syndrome.

机构信息

Department of Internal Medicine III, University Hospital Freiburg, Germany.

出版信息

Resuscitation. 2012 Jun;83(6):715-20. doi: 10.1016/j.resuscitation.2012.01.028. Epub 2012 Feb 1.

DOI:10.1016/j.resuscitation.2012.01.028
PMID:22306259
Abstract

BACKGROUND

The prognosis of immediate survivors of cardiac arrest remains poor, as the majority of these patients develops an inflammatory disorder known as the post-cardiac arrest syndrome (PCAS). Recently, the endothelial glycocalyx has been shown to be a key modulator of vascular permeability and inflammation, but its role in PCAS remains unknown.

METHODS

Plasma levels of the glycocalyx components syndecan-1, heparan sulfate and hyaluronic acid were measured in 25 patients after immediate survival of cardiac arrest during different phases of PCAS. Twelve hemodynamically stable patients with acute coronary syndrome served as controls.

RESULTS

Cardiac arrest resulted in a significant increase in syndecan-1, heparan sulfate and hyaluronic acid levels compared to controls, indicating a shedding of the endothelial glycocalyx as a pathophysiological component of the post cardiac arrest syndrome. The time course differed between the individual glycocalyx components, with a higher increase of syndecan-1 in the early phase of PCAS (2.8-fold increase vs. controls) and a later peak of heparan sulfate (1.7-fold increase) and hyaluronic acid (2-fold increase) in the intermediate phase. Only the plasma levels of syndecan-1 correlated positively with the duration of CPR and negatively with the glycocalyx-protective protease inhibitor antithrombin III. Plasma levels of both syndecan-1 and heparan sulfate were higher in eventual non-survivors than in survivors of cardiac arrest.

CONCLUSION

Our data for the first time demonstrates a perturbation of the endothelial glycocalyx in immediate survivors of cardiac arrest and indicate a potential important role of this endothelial surface layer in the development of post-cardiac arrest syndrome.

摘要

背景

心脏骤停即刻幸存者的预后仍然很差,因为大多数患者会出现一种称为心脏骤停后综合征(PCAS)的炎症性疾病。最近,内皮糖萼已被证明是血管通透性和炎症的关键调节剂,但它在 PCAS 中的作用尚不清楚。

方法

在心脏骤停后即刻存活的 25 例 PCAS 不同阶段的患者中测量了糖萼成分硫酸乙酰肝素、透明质酸和 syndecan-1 的血浆水平。12 例血流动力学稳定的急性冠状动脉综合征患者作为对照。

结果

与对照组相比,心脏骤停导致 syndecan-1、硫酸乙酰肝素和透明质酸水平显著升高,表明内皮糖萼脱落是心脏骤停后综合征的病理生理组成部分。单个糖萼成分的时间过程不同,PCAS 早期 syndecan-1 增加幅度较高(与对照组相比增加 2.8 倍),中期肝素硫酸(增加 1.7 倍)和透明质酸(增加 2 倍)峰值较高。只有 syndecan-1 的血浆水平与 CPR 的持续时间呈正相关,与糖萼保护蛋白酶抑制剂抗凝血酶 III 呈负相关。心脏骤停最终幸存者的 syndecan-1 和肝素硫酸血浆水平均高于幸存者。

结论

我们的数据首次证明了心脏骤停即刻幸存者内皮糖萼的紊乱,并表明该内皮表面层在心脏骤停后综合征的发展中可能具有重要作用。

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