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 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.
瞄准：调查在门静脉高血压之间的相互作用，由由测量类型的表示在门hypertensive vasculopathy 的致病观察脾的动脉、静脉的病理学的变化和细胞外的矩阵的 ro1e 的内脏的亢奋的动态循环和内脏的 vasculopathy 我和在门hypertensive 病人的脾的静脉的墙中的类型 III 职业人员骨胶原 mRNA 。方法：从门 hypertensive 病人(n=20 ) 和正常控制(n=10 ) 拿的脾的动脉和静脉的词法变化被观察在下面光并且电子显微镜。全部的 RNA 被提取并且我和在门 hypertensive 病人(n=20 ) 的脾的静脉的墙中的类型 III 专业版骨胶原 mRNA 是的类型的表达式用反向的抄写聚合酶链反应(RT-PCR ) 检测的半份量上。结果：在光显微镜下面，脾的动脉的内膜被破坏，内部有弹性的膜和脾的动脉的墙的中间的弹性纤维被堕落并且碎。脾的静脉的内膜变得显著地厚。Endothelia1 房间不与附壁血栓的形成是未经触动的。大桶集成通信适配器媒介变得由于平滑肌的肥大显著地变厚。纤维和结缔组织显然被增加。在电子显微镜下面，脾的动脉的平滑肌房间被堕落并且 necrotized。平滑肌房间的显型变化了从进合成类型紧缩。红细胞和血小板在损坏 endothelial 附近积累了。合成平滑肌房间在脾的静脉和他们的细胞质是占优势的有的丰富的不平的 endoplasmic 核糖体和 Golgi。沿着脉管的墙，很多骨胶原纤维被扔，内膜被损坏，血部件积累了。在类型的表示没有有效差量我在在有没有门静脉高血压( P>0.05 )的门静脉高血压和那些的病人之间的脾的静脉的墙中的职业人员骨胶原 mRNA ，但是没有门静脉高血压( P<0.01 )，类型 III procoagen mRNA 的表示比在那些在有门静脉高血压的病人是显著地更强壮的。结论：类型 III 职业人员骨胶原和骨胶原可能是重要细胞外的矩阵导致 neointimal 形成并且在门 hypertensive vasculopathy 的致病的脉管的改变。在脾的动脉和静脉的病理学的变化在门静脉高血压病人存在。可能在门静脉高血压，内脏的亢奋的动态发行量和内脏的 vasculopathy 之间有一个相互作用。
基金
Supported by National Natural Science Foundation of China, No. A30170920
