Systemic endothelial activation is greater in septic than in traumatic-hemorrhagic shock but does not correlate with endothelial activation in skin biopsies
Systemic endothelial activation is greater in septic than in traumatic-hemorrhagic shock but does not correlate with endothelial activation in skin biopsies
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DOI：
10.1097/00003246-200204000-00015
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发表时间：
2002-04-01
影响因子：
8.8
通讯作者：
Dignat-George, F
中科院分区：
文献类型：
--
作者：
Leone, M;Boutière, B;Dignat-George, F
目的：脓毒症和严重创伤导致内皮细胞活化和损伤。活化的内皮细胞表达控制白细胞迁移的黏附受体。活化后，一些黏附分子也以可溶性形式释放到血浆中。本研究旨在比较三组患者可溶性细胞黏附分子（sCAMs）的表达：脓毒性休克患者、严重脓毒症患者和创伤失血性休克患者。此外，还在皮肤活检中检测了这些黏附分子在内皮细胞上的表达。
设计：前瞻性观察研究
地点：一所大学医院的重症监护病房
患者：研究包括15例脓毒性休克患者（根据Bone的定义）、11例严重脓毒症患者（根据Bone的定义）和13例创伤失血性休克患者。15名健康献血者作为对照。
测量和主要结果：在疾病的第1、2和3天对sCAMs进行测量。第1天，与对照组相比，脓毒性休克患者的sE -选择素、sP -选择素、可溶性血管细胞黏附分子（sVCAM）-1和可溶性细胞间黏附分子（sICAM）-1显著升高，而创伤失血性休克患者中除sP -选择素外，这些sCAMs均在正常范围内。在严重脓毒症患者（脓毒症连续过程中比脓毒性休克更早的阶段）中，发现sCAMs的值处于中间水平。在脓毒性休克患者的皮肤活检中，内皮细胞对组成性内皮分子（CD146、CD144、CD131）呈强染色。诱导性分子（ICAM - 1、VCAM - 1和E -选择素）呈强染色阳性表达。创伤失血性休克患者的活检显示内皮分子有类似的阳性表达。
结论：sCAMs的模式表明，内皮细胞的系统性活化在三种临床情况中是不同的，在脓毒性休克中最强，在严重脓毒症中处于中间水平，在创伤失血性休克中与对照组无差异。皮肤活检所证明的类似内皮细胞活化情况表明，在解释血浆中的CAMs时需要谨慎，因为它不一定反映内皮细胞的原位活化状态。（《重症医学》2002年；30:808 - 814）
Objective: Sepsis and severe trauma result in endothelial activation and damage. The activated endothelium expresses adhesion receptors that control leukocyte trafficking. After activation, some adhesion molecules are also released into plasma as soluble forms. The present study was designed to compare the expression of soluble cell adhesion molecules (sCAMs) in three groups of patients: those with septic shock, severe sepsis, and traumatic-hemorrhagic shock. In addition, the endothelial expression of these adhesive molecules was examined in skin biopsies.Design: Prospective observational studySetting: Intensive care unit at a university hospitalPatients: The study included 15 patients with septic shock (by Bone's definition), 11 patients with severe sepsis (by Bone's definition), and 13 patients with traumatic-hemorrhagic shock. Fifteen healthy blood donors served as controls.Measurements and Main Results: Measurements of sCAMs were performed on days 1, 2, and 3 of the disease. On day 1, when compared with controls, sE-selectin, sP-selectin, soluble vascular cell adhesion molecule (sVCAM)-1, and soluble intercellular adhesion molecule (sICAM)-1 were markedly elevated in septic shock patients, whereas these sCAMS, except for sP-selectin, were within normal ranges in traumatic-hemorrhagic shock patients. In patients with severe sepsis, an earlier stage than septic shock in the sepsis continuum, intermediate values of sCAMS were found. In skin biopsies of septic shock patients, the endothelial cells expressed a bright staining of constitutive endothelial molecules (CD146, CD144, CD131). Inducible molecules (ICAM-1, VCAM-1, and E-selectin) were positively expressed with bright staining. The biopsies from traumatic-hemorrhagic shock patients showed a similar positive expression of endothelial molecules.Conclusion: The patterns of sCAMS; indicate that the systemic activation of the endothelium is different in the three clinical entities, maximum in septic shock, intermediate in severe sepsis, and not different from controls in traumatic-hemorrhagic shock. Comparable endothelial activation as evidenced by skin biopsies suggests that caution is required in the interpretation of CAMs in plasma, which does not necessarily reflect the in situ activation state of endothelium. (Crit Care Med 2002; 30:808-814).