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首页> 外文期刊>Neurosurgery >Endothelial cell activation after subarachnoid hemorrhage.
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Endothelial cell activation after subarachnoid hemorrhage.

机译：蛛网膜下腔出血后内皮细胞活化。

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OBJECTIVE: Evidence from animal experiments suggests that endothelial cell activation plays a pathogenetic role in the development of cerebral ischemia after subarachnoid hemorrhage (SAH). We measured plasma concentrations of two markers of endothelial cell activation, i.e., ED1-fibronectin (ED1-fn) and von Willebrand factor (vWf), among patients with aneurysmal SAH. We analyzed the relationships of concentrations to initial clinical conditions, treatment modalities, and the occurrence of delayed cerebral ischemia. METHODS: We collected 123 blood samples from 27 patients with aneurysmal SAH. Aneurysms were treated surgically in 19 cases, were treated endovascularly in 7 cases, and remained untreated in 1 case. Twelve patients developed symptomatic delayed cerebral ischemia. RESULTS: Initial concentrations of ED1-fn (4.3 +/- 3.7 microg/ml) and vWf (17.8 +/- 8.2 microg/ml) were higher than the reference values (ED1-fn, 1.7 +/- 0.9 microg/ml, P < 0.001; vWf, 11.5 +/- 5.2 microg/ml, P = 0.003). Concentrations were higher among patients in poor clinical condition at admission, compared with patients in good clinical condition (mean difference, ED1-fn, 5.7 microg/ml, P = 0.04; vWf, 10.4 microg/ml, P = 0.02). Levels of both markers increased significantly after surgery (mean increase, ED1-fn, 7.5 microg/ml, P = 0.01; vWf, 13.2 microg/ml, P = 0.05) and after ischemic episodes (mean increase, ED1-fn, 8.3 microg/ml, P = 0.02; vWf, 5.0 microg/ml, P = 0.04). CONCLUSION: Plasma concentrations of markers of endothelial cell activation were increased early after SAH and were significantly associated with the clinical condition at admission. We also observed a significant increase in concentrations after surgery and after ischemic episodes. Whether endothelial cell activation is a causal or indirectly related factor in the pathogenesis of delayed cerebral ischemia after SAH is still uncertain.
机译：目的：动物实验的证据表明，内皮细胞活化在蛛网膜下腔出血（SAH）后脑缺血的发展中具有致病作用。我们在患有动脉瘤的SAH患者中测量了两种内皮细胞激活标志物的血浆浓度，即ED1-纤连蛋白（ED1-fn）和von Willebrand因子（vWf）。我们分析了浓度与初始临床状况，治疗方式和迟发性脑缺血的关系。方法：我们从27例动脉瘤性SAH患者中收集了123份血液样本。手术治疗动脉瘤19例，血管内治疗7例，未治疗1例。 12名患者出现症状性迟发性脑缺血。结果：ED1-fn（4.3 +/- 3.7 microg / ml）和vWf（17.8 +/- 8.2 microg / ml）的初始浓度高于参考值（ED1-fn，1.7 +/- 0.9 microg / ml， P <0.001; vWf，11.5 +/- 5.2 microg / ml，P = 0.003）。与临床状况良好的患者相比，入院时临床状况较差的患者中的浓度更高（平均值差异，ED1-fn为5.7 microg / ml，P = 0.04; vWf为10.4 microg / ml，P = 0.02）。手术后和缺血发作后，两种标志物的水平均显着升高（平均升高，ED1-fn，7.5 microg / ml，P = 0.01; vWf，13.2 microg / ml，P = 0.05），并且缺血发作后（平均升高，ED1-fn，8.3 microg） /ml，P＝0.02;vWf，5.0μg/ml，P＝0.04）。结论：SAH后早期内皮细胞激活标志物的血浆浓度升高，并且与入院时的临床状况显着相关。我们还观察到手术后和缺血发作后血药浓度显着增加。在SAH后延迟性脑缺血的发病机制中，内皮细胞激活是因果还是间接相关因素尚不确定。

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