脳血管障害の最先端　　くも膜下出血における血管内皮細胞障害―血管内手術と開頭手術の比較―:―血管内手術と開頭手術の比較―

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Endovascular coil emobolization has emerged as an alternative treatment of ruptured intracranial aneurysms, and it has reduced the therapeutic assault on vessels. However, it is not clear what happens between such therapeutic assault and vascular response on a molecular level. We investigated endothelial cell disorder after subarachnoid hemorrhage (SAH) and the impact of open and endovascular surgery. In rat SAH models, we confirmed the endothelial perturbation such as the expression of interleukin 1-β, plasminogen actibator inhibitor-1 (PAI-1), von Willebrand factor (vWF), E-selectin, and apoptosis-related products that caused the morphological changes of endothelial cells. In a real-time RT-PCR study, direct brain damage by a cold injury after experimental SAH emphasized the expression of p38 mitogen-activated protein kinase (p38 MAPK) in endothelial cells. In 36 SAH patients, the serum markers of endothelial cell disorder such as PAI-1, vWF and E-selectin that exist in the lower stream of p38 MAPK were compared between endovascular coil embolization (18 patients) and open surgery (18 patients). The levels of serum markers of endothelial cell disorder in open surgery were statistically higher than endovascular surgery (p<0.05). These results indicate that the therapeutic assault on the endothelial cells in open surgery may be higher than that in endovascular coil embolization.
一般社団法人日本脳卒中の外科学会の論文