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肝癌自发性破裂患者血管超微结构研究

Ultrastructure study on patients with spontaneous rupture of hepatocellular carcinoma

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【作者】 朱立新耿小平范上达

【Author】 ZHU Li-xin, GENG Xiao-ping, FAN Shang-da. Department of Surgery, Affiliated Hospital of Anhui Medical University, Hefei 230022, China

【机构】 安徽医科大学附属医院普外科安徽医科大学附属医院普外科香港大学外科学系

【摘要】 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。

【Abstract】 Objective To investigate the ultrastructure of small artery wall in patients with spontaneous rupture of hepatocellular carcinoma (HCC). Methods Transmission electron microscopy was used to study 11 specimens from ruptured HCC and 11 cases with non-ruptured HCC. Results The phenomenon of activated phagocytosis in macrophage could be found in 3 cases with ruptured HCC and 10 cases with non-ruptured HCC, respectively (P<0.05). In 9 specimens with ruptured HCC, the evidence of vascular injury characterized as less cell junctions and larger fenestres in endothelial cells, broken elastic lamina, proliferated and fragmented elastin and damaged structure of collagen was found in small arteries. The phenomenon of electron-dense deposit in the elastic lamina, and signs of more protein synthesis in endothelial cells were also present in these specimens. In the patients with non-ruptured HCC, the evidence of vascular injury can be found only in 2 cases (P<0.01). Less cell junctions and larger fenestres could increase the permeability of vascular wall. The electron-dense deposition in elastic lamina may represent the deposition of antigen-antibody complex in elastic membrane which had been found in our previous study. The vascular injury was postulated to be caused by the deposition of antigen-antibody complex in vascular wall which was identified by our previous study. The vascular wall in the patient with ruptured HCC could become stiff and weak due to the proliferated fragment elastin and damaged collagen which would make the blood vessels more prone to splitting and result in hemorrhage and the rupture of HCC. Conclusions The vascular injury caused by antigen-antibody complex deposition might related to the spontaneous rupture of HCC.

【基金】 安徽省自然科学基金资助项目(03043702)
  • 【文献出处】 中华外科杂志 ,Chinese Journal of Surgery , 编辑部邮箱 ,2006年03期
  • 【分类号】R735.7
  • 【被引频次】30
  • 【下载频次】154
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