Fujisawa H, Ito H, Saito K, Ikeda K, Nitta H, Yamashita J
Department of Neurosurgery, Yamaguchi University School of Medicine, Ube, Japan.
Surg Neurol. 1991 Jun;35(6):441-5. doi: 10.1016/0090-3019(91)90177-b.
Capsules of chronic subdural hematoma were immunohistochemically stained with monoclonal antibody against tissue-type plasminogen activator. Endothelial cells of sinusoids and capillaries in the outer membrane showed strong immunostaining. Endothelial cells of veins and arteries in the dura mater showed moderate and weak staining. No cells other than the endothelial cells were stained. In the inner membrane, tissue-type plasminogen activator immunoreactivity was not seen. The mean concentration of tissue-type plasminogen activator in the hematoma content was higher than that in the plasma. The more the sinusoids in the outer membrane were developed, the higher the concentration of tissue-type plasminogen activator contained in the hematoma fluid. In chronic subdural hematoma, overproduction and oversecretion of tissue-type plasminogen activator from the sinusoidal and capillary endothelial cells in the outer membrane cause increased fibrinolysis, which in turn impairs hemostasis, and hemorrhage from the capillaries recurs, resulting in enlargement of the chronic subdural hematoma.
采用抗组织型纤溶酶原激活剂单克隆抗体对慢性硬膜下血肿包膜进行免疫组织化学染色。外膜中窦状隙和毛细血管的内皮细胞呈现强免疫染色。硬脑膜中静脉和动脉的内皮细胞呈现中度和弱染色。除内皮细胞外无其他细胞被染色。在内膜中，未见到组织型纤溶酶原激活剂免疫反应性。血肿内容物中组织型纤溶酶原激活剂的平均浓度高于血浆中的浓度。外膜中窦状隙越发达，血肿液中所含组织型纤溶酶原激活剂的浓度越高。在慢性硬膜下血肿中，外膜中窦状隙和毛细血管内皮细胞过度产生和分泌组织型纤溶酶原激活剂导致纤维蛋白溶解增加，进而损害止血功能，毛细血管反复出血，导致慢性硬膜下血肿增大。
