Murakami Hideki, Hirose Yuichi, Sagoh Masachika, Shimizu Kazuhiro, Kojima Masaru, Gotoh Kazuhiro, Mine Yutaka, Hayashi Takuro, Kawase Takeshi
Department of Neurosurgery and Pathology, Ashikaga Red Cross Hospital, Ashikaga-city, Tochigi, Japan.
J Neurosurg. 2002 May;96(5):877-84. doi: 10.3171/jns.2002.96.5.0877.
Thrombomodulin is a thrombin receptor on vascular endothelial cells that is highly expressed when these cells are injured, and it has anticoagulating activity. The authors investigated thrombomodulin expression to clarify why chronic subdural hematomas (CSDHs) continue to grow slowly, like a tumor, and are liquefied.
Burr hole craniotomy and drainage were performed in all 35 patients with CSDH who were included in the study. The plasma-soluble thrombomodulin and blood clotting factor values were determined in the hematoma and in peripheral blood. In the seven most recent cases, the plasma-soluble thrombomodulin values were determined in the residual hematoma collected from the drainage tube the day after surgery. The outer membranes of the CSDH that were obtained as specimens at operation were stained with monoclonal antibody against thrombomodulin for immunohistochemical studies. The plasma-soluble thrombomodulin values were higher (p < 0.0001), and conversely the values for factors V and VIII were lower in the hematoma than in peripheral blood (p < 0.0001). The plasma-soluble thrombomodulin values were lower in the residual hematomas than in the same lesions at operation (p = 0.018). The endothelial cells on the sinusoidal vessels exhibited immunoreactivity with thrombomodulin antibody in 28 (93%) of 30 cases.
The thrombomodulin is expressed on the sinusoidal vessels, and the blood coagulation system is inhibited in the hematoma. These findings indicate that these vessels are continuously injured and fail to heal. As a result, the bleeding from the sinusoidal vessels may persist, and the hematoma may grow slowly and fail to coagulate. It is suspected that transmitted pulsation variations in the hematoma cavity generate sinusoidal vessel injury.
血栓调节蛋白是血管内皮细胞上的一种凝血酶受体,当这些细胞受损时会高度表达,且具有抗凝活性。作者研究血栓调节蛋白的表达,以阐明慢性硬膜下血肿(CSDH)为何像肿瘤一样持续缓慢生长并液化。
对纳入研究的35例CSDH患者均行钻孔开颅引流术。测定血肿及外周血中的血浆可溶性血栓调节蛋白和凝血因子值。在最近的7例病例中,于术后第1天从引流管收集的残余血肿中测定血浆可溶性血栓调节蛋白值。将手术中获取的CSDH外膜标本用抗血栓调节蛋白单克隆抗体染色,进行免疫组织化学研究。血肿中的血浆可溶性血栓调节蛋白值较高(p<0.0001),相反,因子V和VIII的值在血肿中低于外周血(p<0.0001)。残余血肿中的血浆可溶性血栓调节蛋白值低于手术时同一病变中的值(p = 0.018)。在30例病例中的28例(93%),窦状血管上的内皮细胞与血栓调节蛋白抗体呈免疫反应。
血栓调节蛋白在窦状血管上表达,血肿中的凝血系统受到抑制。这些发现表明这些血管持续受损且无法愈合。因此,窦状血管可能持续出血,血肿可能缓慢生长且无法凝固。怀疑血肿腔内传递的搏动变化导致窦状血管损伤。