| When we study on portal hypertension ( PHT ) ,we can find that those patients with portal hypertension have pathologic change of vascular in potal vein systerm besides derangement of hemodynamics,it can be called potal hypertension vascular lesion and it is very important of procession in PHT. Now, we have found that many growth factors and cellular factors could promote vascular formation. But in many vascular growth factors, vascular endothelial cell growth factor(VEGF)is the most important vascular growth factor. Vascular endothelial cell growth factor(VEGF)is a kind of glucoprotein ,which has separated by culturing stellate cells of bovine glandula pituitaria in vitro by Ferrara etc. in 1989.lt can express that anxo-act vascular endothelial cell growth specificly and induce vasotropic growth ,so it is called VEGF.VEGF can facilitate endothelial proliferation strongly and vasotropic growth with conjugating vascular endothelial cell's specific receptor.Its biological characteristic express two ways: increase wall of micrangium's permeability and conjugate vascular endothelial cell's specificreceptor, anxo-act vascular endothelial cell cleavage and proliferation, so lead to formate neogenetic vascular. During potal hypertension(PHT),internal organ including spleen happen to hyperdynamtic circulatory state, increasing volume and velocity of blood flow, and elevating side-pressure of vessel wall. These mechanical actions can injury vascular endothelial cell, damage intaction of vascular wall, and precipitate proliferation of smooth muscle cell and ground substance -lead to vascular pathological process. The mRNA of VEGF in spleen was highly expressed during potal hypertension. VEGF can anxo-act vascular endothelial cell proliferation and increase permeability of wall of vessel strongly. Proliferating of vessel and increasing storage of volume of blood flow in spleen can result in high pressure of splenic pulp. By these ways, they can exacerbate portal hypertension state and hypersplenism syndrome. So VEGF is an important reason during anamorphism of hepatocirrhosis. In this study, we observed expression of the mRNA of VEGF in wistar white rats' spleen in different period of hepatocirrhosis with in situ hybridization, and discovered the effect of VEGF in portal hypertension due to cirrhosis.Methods: Apinoid wistar white rats ,quality standard was about 200 ?30 gram (belong to SPF animal in experimental animal center ,FMMU)were randomly divided into experimental group (eighteen rats) and control group (six rats).Experimental group was gived hypodermic injection at a dose of 0.3ml/100g by 60 percent carbon tetrachloride olive solution every four days and drinked 50ml/L ethyl alcohol. we would divide course of cirrhotic rats models into three stages : early stage (the 25th day) is fatty degenerationnecrosis ;middle stage (the 45th day) is proliferation of fibrous tissue ; advanced stage (the 65th day) is formation of pseudolobuli . Control group was gived hypodermic injection at a dose of 0.3ml/100g by olive solution every four days and drinked water . All rats were cut their head and killed . Their spleens were refrigerated storage in ?173 C liquid nitrogen quickly . The mRNA of VEGF was identified with in situ hybridization . Judgement standard: Divided them into three ranks by the depth of coloration and quantity of positive granule . Positive sectiones were thought that positive granule occupy 30 percent every high power field . Every specimen was mad five sectiones continuously and was stained. If we found one positive slice among them , we could think it is positive case .Results: The mRNA of VEGF in cirrhotic rats with portal hypertension was highly expressed: Early stage was 50 percent (3/6), middle stage is 66.7 (4/6) ,advanced stage was 100 percent (6/6) .On the contrary , expression in control group was about 16.7 (1/6) , only one case was slight positive . we could draw a conclusion P <0.05 by Fisher's exact test.Conclusions: (1) The more serious the degree of portal hypertens...
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