Bitsch A, Klene W, Murtada L, Prange H, Rieckmann P
Department of Neurology, Georg-August-University, Göttingen, Germany
Stroke. 1998 Oct;29(10):2129-35. doi: 10.1161/01.str.29.10.2129.
Activation of endothelial cells is a consequence of cerebral ischemia and leads to the expression of adhesion molecules such as intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin, which can be released into the blood. This study aimed to define the kinetics of soluble adhesion molecule serum levels after cerebral ischemia and their correlation with the extent of neurological deficits, clinical outcome, and infarct volume as measured on CT scans. Methods-Plasma levels of soluble (s) ICAM-1, sVCAM-1, and sE-selectin were repeatedly determined by ELISA in 38 patients during a period of 14 days after acute cerebral ischemia.
Soluble adhesion molecule levels demonstrated considerable variability. Overall, concentrations revealed characteristic and significant changes after completed strokes but not after transient ischemic attacks. In patients with completed stroke (n=26) but not in patients with transient ischemic attacks (n=12), sICAM-1 peaked within 24 hours (P=0.04), sVCAM-1 reached a maximum after 5 days (P=0.02), and sE-selectin levels decreased after 5 days (P=0.002). There was no clear-cut correlation of soluble adhesion molecule levels with infarct volume or clinical disability. The initial increase of sE-selectin levels was higher in more disabled patients (P=0.02). sICAM-1 levels were higher in patients with signs of infection (n=9; P=0.03).
As a result of large interindividual variability influenced by ischemia-independent factors, soluble adhesion molecules are not reliable candidates as surrogate markers in acute cerebral ischemia. The characteristic profile of individual soluble adhesion molecules after completed stroke supports prior hypotheses of their involvement in the pathogenesis of acute cerebral ischemia, but this needs to be clarified in detail.
内皮细胞激活是脑缺血的一个后果，会导致细胞间黏附分子1（ICAM-1）、血管细胞黏附分子1（VCAM-1）和E-选择素等黏附分子的表达，这些分子可释放到血液中。本研究旨在确定脑缺血后可溶性黏附分子血清水平的变化动力学，以及它们与神经功能缺损程度、临床结局和CT扫描测量的梗死体积之间的相关性。方法：通过酶联免疫吸附测定法（ELISA）在38例急性脑缺血患者发病后14天内反复测定其血浆中可溶性（s）ICAM-1、sVCAM-1和sE-选择素的水平。
可溶性黏附分子水平表现出相当大的变异性。总体而言，在完全性卒中后浓度显示出特征性且显著的变化，但短暂性脑缺血发作后则不然。在完全性卒中患者（n = 26）中，而非短暂性脑缺血发作患者（n = 12）中，sICAM-1在24小时内达到峰值（P = 0.04），sVCAM-1在5天后达到最大值（P = 0.02），sE-选择素水平在5天后下降（P = 0.002）。可溶性黏附分子水平与梗死体积或临床残疾之间没有明确的相关性。在残疾程度更高的患者中，sE-选择素水平的初始升高更高（P = 0.02）。在有感染迹象的患者中sICAM-1水平更高（n = 9；P = 0.03）。
由于受缺血无关因素影响个体间差异较大，可溶性黏附分子在急性脑缺血中作为替代标志物并不可靠。完全性卒中后个体可溶性黏附分子的特征性变化支持了其参与急性脑缺血发病机制的先前假设，但这需要详细阐明。
