Lengyel I, Acsády G
Clinic of Cardiovascular Surgery, Semmelweis Medical University, Budapest, Hungary.
Acta Morphol Hung. 1990;38(3-4):259-67.
The authors should like to contribute to the unsettled problem of the development of varicose venous disease with their own experience. They evaluate parallel the histomorphological observations and certain pathobiochemical changes which can be recognized in exstirpated varicose veins. Fourty five stripped saphenas have been studied. They were divided into two groups: a macroscopically normal and a varicose one. The varicose patients were divided again into two subsamples according to the occurrence or lack of thrombophlebitis in their medical case history. The authors were looking for the appropriate pathobiochemical changes of the vessel walls running parallel to the usual histopathological changes. It seems quite possible that the effect which triggers the development of the disease could be anything which causes hypoxia, alters the energy metabolism of the otherwise bradytrophic vascular tissues. Accumulation of proteoglycans, as well as collagen and elastic fibers in place of the smooth muscle cells may cause a decrease in the elasticity of the veins and may produce favourable conditions to thrombus formation and local inflammation.
作者们希望凭借自身经验,为静脉曲张性疾病发展这一尚未解决的问题贡献力量。他们同时评估了在切除的曲张静脉中可识别的组织形态学观察结果和某些病理生化变化。对45条剥脱的大隐静脉进行了研究。它们被分为两组:一组宏观上正常,另一组曲张。静脉曲张患者又根据其病史中是否存在血栓性静脉炎分为两个子样本。作者们在寻找与常见组织病理学变化平行的血管壁的适当病理生化变化。引发该疾病发展的因素很可能是任何导致缺氧、改变原本营养缓慢的血管组织能量代谢的因素。蛋白聚糖以及胶原蛋白和弹性纤维取代平滑肌细胞的积聚可能会导致静脉弹性下降,并可能为血栓形成和局部炎症创造有利条件。