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目的通过透射电子显微镜对发生自发性破裂的肝癌小动脉壁进行超微结构检查,进一步证实小动脉病变在肝癌自发性破裂病理变化中的作用。方法对11例肝癌自发性破裂患者的手术标本与同期随机选取的11例肝癌非破裂患者手术标本进行小动脉壁的透射电子显微镜检查。结果3例肝癌自发性破裂的患者存在巨噬细胞吞噬功能活跃的现象,而该现象却存在于10例非破裂患者中。肿瘤破裂的患者中,9例患者的小动脉壁表现出血管受损现象,包括:血管内皮细胞发生细胞连接消失、窗口直径过大、血管内皮显示高蛋白合成征象;血管壁弹力膜断裂、弹性硬蛋白过度增生及胶原纤维结构受损,其弹力膜中可见电子沉淀物。在肿瘤非破裂的患者中,上述血管受损现象仅在2例患者中发现。二组患者的巨噬细胞功能受损及血管受损的发生率有显著性差异。结论肝癌破裂患者中的小动脉病变使其管壁通透性增加、弹性消失及支撑力下降,是发生自发性破裂出血的重要原因。
Objective To investigate the ultrastructural changes of arteriolar wall of spontaneous rupture of hepatocellular carcinoma (HCC) by transmission electron microscope (TEM), further confirming the role of arterioles in pathological changes of spontaneous rupture of liver cancer. Methods Eleven cases of spontaneous rupture of hepatocellular carcinoma were examined by transmission electron microscopy on the arterial wall of 11 patients with non-ruptured hepatocellular carcinoma at random. Results Three patients with spontaneous rupture of liver cancer had phagocytosis of macrophages. However, this phenomenon existed in 10 patients with non-ruptured patients. Among the patients with tumor rupture, the arteriolar wall of 9 patients showed vascular damage, including disappearance of cell junctions in vascular endothelial cells, excessively large window diameter, signs of high protein synthesis in the vascular endothelium, rupture of the elastic membrane of the blood vessel wall, Hard protein hyperplasia and damaged collagen fiber structure, the elastic membrane can be seen electron precipitation. In patients with non-cancerous tumors, the above vascular injury was found only in 2 patients. Two groups of patients with impaired macrophage function and the incidence of vascular damage were significantly different. Conclusions Small artery lesions in patients with ruptured liver cancer increase the permeability of the wall, reduce the elasticity and decrease the supportive force, which is an important cause of spontaneous rupture of the hemorrhage.