Splenic vasculopathy in portal hypertension patients

被引:8
|
作者
Li, Tao [1 ]
Ni, Ji-Yuan [1 ]
Qi, Yan-Wu [1 ]
Li, Hai-Yang [1 ]
Zhang, Tong [1 ]
Yang, Z. [1 ]
机构
[1] Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Hepat Surg, 13 Hangkong Rd, Wuhan 430030, Hubei Province, Peoples R China
关键词
portal hypertension; splanchnic hyperdynamic circulation; splanchnic vasculopathy;
D O I
10.3748/wjg.v12.i17.2737
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
AIM: To investigate the interaction between portal hypertension, splanchnic hyperdynamic circulation and splanchnic vasculopathy by observing splenic arterial and venous pathological changes and the role of extracellular 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. Endothelial 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 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. (C) 2006 The WJG Press. All rights reserved.
引用
收藏
页码:2737 / 2741
页数:5
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