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首页> 外文期刊>World Journal of Gastroenterology >Splenic vasculopathy in portal hypertension patients.
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Splenic vasculopathy in portal hypertension patients.

机译：门静脉高压症患者的脾血管病变。

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AIM: To investigate the interaction between portal hypertension, splanchnic hyperdynamic circulation and splanchnic vasculopathy by observing splenic arterial and venous pathological changes and the ro1e of extra-cellular matrix in the pathogenesis of portal hypertensive vasculopathy by measuring the expression of type I and type III procollagen mRNA in splenic venous walls of portal hypertensive patients. METHODS: Morphological changes of splenic arteries and veins taken from portal hypertensive patients (n=20) and normal controls (n=10) were observed under optical and electron microscope. Total RNA was extracted and the expression of type I and type III procollagen mRNA in splenic venous walls of portal hypertensive patients (n=20) was semi-quantitatively detected using reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Under optical microscope, splenic arterial intima was destroyed and internal elastic membrane and medial elastic fibers of the splenic arterial walls were degenerated and broken. Splenic venous intima became remarkably thick. Endothelia1 cells were not intact with formation of mural thrombus. The tunica media became thickened significantly due to hypertrophy of smooth muscles. Fibers and connective tissues were increased obviously. Under electron microscope, smooth muscle cells of the splenic arteries were degenerated and necrotized. Phenotypes of smooth muscle cells changed from constrictive into synthetic type. Red blood cells and platelets accumulated around the damaged endothelial cells. Synthetic smooth muscle cells were predominant in splenic veins and their cytoplasma had plentiful rough endoplasmic reticulum ribosomes and Golgi bodies. Along the vascular wall, a lot of collagen fibers were deposited, the intima was damaged and blood components accumulated. There was no significant difference in the expression of type I procollagen mRNA in splenic venous wall between the patients with portal hypertension and those without portal hypertension (P>0.05), but the expression of type III procoagen mRNA was significantly stronger in the patients with portal hypertension than in those without portal hypertension (P<0.01). CONCLUSION: Type III procollagen and collagen might be important extra-cellular matrix resulting in neointimal formation and vascular remodeling in the pathogenesis of portal hypertensive vasculopathy. The pathological changes in splenic arteries and veins exist in portal hypertension patients. There might be an interaction between portal hypertension, splanchnic hyperdynamic circulation and splanchnic vasculopathy.
机译：目的：通过测量I型和III型前胶原的表达，观察脾动脉和静脉的病理变化以及门脉高压性血管病发病机理中细胞外基质的作用，从而探讨门脉高压，内脏高动力循环和内脏血管病变之间的相互作用。门脉高压患者脾静脉壁的mRNA。方法：在光学和电子显微镜下观察门静脉高压患者（n = 20）和正常对照组（n = 10）的脾动脉和静脉的形态变化。提取总RNA，并使用逆转录-聚合酶链反应（RT-PCR）半定量检测门静脉高压症患者（n = 20）脾壁中I型和III型前胶原mRNA的表达。结果：在光学显微镜下，脾动脉内膜被破坏，脾动脉壁的内部弹性膜和内侧弹性纤维变性并断裂。脾静脉内膜明显变厚。内皮细胞未完整形成壁血栓。由于平滑肌肥大，中膜明显增厚。纤维和结缔组织明显增加。在电子显微镜下，脾动脉的平滑肌细胞退化并坏死。平滑肌细胞的表型从收缩型转变为合成型。红细胞和血小板聚集在受损的内皮细胞周围。脾静脉中主要是合成的平滑肌细胞，其细胞质中有大量粗糙的内质网核糖体和高尔基体。沿血管壁沉积了大量胶原纤维，内膜受到破坏，血液成分积聚。门静脉高压症患者和非门静脉高压症患者的脾静脉壁中I型胶原蛋白mRNA表达无明显差异（P> 0.05），但门静脉高压症患者中III型胶原蛋白mRNA的表达明显增强。高血压患者比没有门静脉高压症的患者高（P <0.01）。结论：III型胶原原和胶原可能是重要的细胞外基质，在门脉高压性血管病的发病机理中导致新内膜形成和血管重塑。门静脉高压症患者存在脾动脉和静脉的病理变化。门脉高压，内脏高动力循环和内脏血管病变之间可能存在相互作用。

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