首页> 外文期刊>Journal of neurosurgery. >Why do chronic subdural hematomas continue to grow slowly and not coagulate? Role of thrombomodulin in the mechanism.
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Why do chronic subdural hematomas continue to grow slowly and not coagulate? Role of thrombomodulin in the mechanism.

机译:为什么慢性硬膜下血肿继续缓慢生长而不凝结?血栓调节蛋白在该机制中的作用。

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OBJECT: 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. METHODS: 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. CONCLUSIONS: 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.
机译:目的:凝血调节蛋白是血管内皮细胞上的凝血酶受体,当这些细胞受到损伤时会高度表达,并具有抗凝活性。作者研究了血栓调节蛋白的表达,以阐明为什么慢性硬膜下血肿(CSDH)像肿瘤一样继续缓慢生长并被液化。方法:对纳入研究的全部35名CSDH患者进行了开颅钻孔和引流。在血肿和外周血中测定血浆可溶性血栓调节蛋白和凝血因子值。在最近的七个病例中,在术后第二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。作为手术标本的CSDH外膜用抗血栓调节蛋白的单克隆抗体染色,用于免疫组织化学研究。血浆中的血浆可溶血栓调节蛋白值较高(p <0.0001),相反,血肿中血浆V和VIII的值低于外周血(p <0.0001)。残余血肿中的血浆可溶性血栓调节蛋白值低于术中相同病变的血浆中血栓调节蛋白值(p = 0.018)。 30例中的28例(93%)中,正弦血管上的内皮细胞与血栓调节蛋白抗体表现出免疫反应性。结论:血栓调节蛋白在正弦血管中表达,血肿中的凝血系统受到抑制。这些发现表明这些血管不断受伤且无法愈合。结果,可能会持续出现来自窦状血管的出血,并且血肿可能会缓慢生长并且无法凝结。怀疑血肿腔中传递的搏动变化会引起正弦血管损伤。

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