Hirsch H E, Blanco C E, Parks M E
J Neuropathol Exp Neurol. 1981 May;40(3):271-80. doi: 10.1097/00005072-198105000-00005.
Recent work has implicated plasminogen activator released from macrophages as a possible mediator of the demyelinating process in experimental allergic encephalomyelitis and multiple sclerosis (MS). We have studied the capacity of white matter and plaques from MS patients to break down fibrin clots, using a histochemical technique. Fibrinolytic activity was localized exclusively to areas around blood vessels and capillaries in both patients and controls. While there was marked variation between individuals, the unaffected white matter from MS patients was, on the average, not more active than that of controls, but plaques tended to show more numerous foci of lysis, often also more intense, than adjacent white matter; there was no correlation with disease activity or age of the plaques as determined by histological criteria. The localization and degree of fibrinolysis observed were not related to the presence of lymphocytic infiltrates, gliosis, or macrophages. However, the findings do not exclude an involvement of fibrinolytic enzymes (although originating from vascular endothelium rather than macrophages) in the genesis of the MS plaque, which commonly starts around a small vein.
近期的研究表明，巨噬细胞释放的纤溶酶原激活物可能是实验性变应性脑脊髓炎和多发性硬化症（MS）脱髓鞘过程的一种介质。我们采用组织化学技术研究了MS患者白质和斑块溶解纤维蛋白凝块的能力。纤溶活性仅定位于患者和对照组血管及毛细血管周围区域。虽然个体之间存在显著差异，但MS患者未受影响的白质平均而言并不比对照组更活跃，不过斑块往往比相邻白质显示出更多的溶解灶，且通常也更强烈；根据组织学标准，这与疾病活动度或斑块年龄无关。观察到的纤溶定位和程度与淋巴细胞浸润、胶质细胞增生或巨噬细胞的存在无关。然而，这些发现并不排除纤溶酶（尽管源自血管内皮而非巨噬细胞）参与MS斑块的形成，MS斑块通常始于一条小静脉周围。
