论文部分内容阅读
目的 研究肝硬化门静脉高压症患者脾静脉和胃冠状静脉壁类粥样硬化样改变，并探讨其发生机理及临床意义。方法 ５０ 例肝硬化门静脉高压症患者，在行脾切除贲门周围血管离断术时取一段脾静脉和胃冠状静脉供研究，１０ 例十二指肠球部溃疡患者和１０ 例外伤性脾破裂患者（ 均无肝硬化） 为对照组，行光镜和电镜观察。结果 光镜见病变组脾静脉和胃冠状静脉壁显著增厚，内皮细胞不完整，形成许多增生结节，呈丘状、乳头状或弥漫性增厚，内膜下间隙有大量排列方向紊乱的平滑肌细胞和聚积大量纤维结缔组织，及呈“糜粥”状坏死、崩解的组织；中膜平滑肌细胞显著增厚，并向内膜下迁移。电镜见内皮细胞破损，附壁血栓形成，内膜下间隙有大量增殖的平滑肌细胞和胶原纤维；中膜和迁移到内膜的平滑肌细胞的表型从收缩型向合成型转化。结论 门脉高压时脾静脉和胃冠状静脉壁中膜平滑肌细胞增殖，迁移和表型改变，从而形成类粥样硬化样斑块，使管壁粗糙、增厚、变硬，故可增加血流阻力和形成附壁血栓。
Objective To study the changes of wall-like atherosclerosis in splenic vein and gastric coronary vein in patients with cirrhosis and portal hypertension and to investigate its mechanism and clinical significance. Methods A total of 50 patients with cirrhosis and portal hypertension were enrolled in this study. A splenic vein and gastric venous coronary vein were obtained during the splenectomy and pericardial vascular disconnection. Ten patients with duodenal ulcer and 10 patients with traumatic rupture (No cirrhosis) as the control group, under light and electron microscopy. Results In the light microscope, the splenic vein and gastric coronary vein wall were significantly thicker and the endothelial cells were incomplete. There were many hyperplastic nodules with moundy, papillary or diffuse thickening. There were a large number of disorders in the subintimal space Smooth muscle cells and accumulation of a large number of fibrous connective tissue, and was “porridge” -like necrosis and disintegration of the organization; medium smooth muscle cells significantly thickening, and the migration to the intima. Electron microscope, endothelial cell damage, mural thrombosis, subtimal space with a large number of proliferation of smooth muscle cells and collagen fibers; and the migration of endometrial smooth muscle cells phenotype from the contraction to the synthesis of transformation. Conclusions The proliferation, migration and phenotypic changes of the smooth muscle cells in the splenic vein and the gastric venous wall of the splenic vein at the portal hypertension may result in the formation of atherosclerotic plaque, which results in rough, thickening and stiffening of the vessel wall, thus increasing blood flow Resistance and formation of mural thrombus.