Scandinavian journal of gastroenterology · 2009
A modified canine model of portal hypertension with hypersplenism.
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Chen Yunzhi, Zhang Qiyu, Liao Yi, Guo Fang, Zhang Yi, Zeng Qiqiang, Jin Wangxun, Shi Hongqi, Zhou Mengtao
Аннотация
OBJECTIVE: The aim of this study was to develop and describe an experimental canine model of portal hypertension with hypersplenism.
MATERIAL AND METHODS: Twenty-five dogs were used randomly divided into three groups: group I (control group, n = 5), group II (PVS, n = 10) and group III (PVS + SVS, n = 10). Portal vein stenosis (PVS) was performed in dogs of group II; in group III dogs the model was first prepared by PVS and additional splenic vein stenosis 3 weeks later (PVS + SVS). Portal vein pressure (PVP), length of spleen and fluctuation of hematocyte counts were measured and recorded at the appointed times. Surgery permitted visual verification of portosystemic collateral circulation. Histopathological variation of the spleen and condition of the bone marrow hyperplasia were examined to confirm the development of hypersplenism.
RESULT: Both group II and group III developed prehepatic portal hypertension; group III also presented satisfactory hypersplenism compared to the control group and group II, as documented at surgery and by hematologic and pathologic examination.
CONCLUSIONS: Based on this study, the modified model of portal hypertension (by PVS + SVS) appears appropriate when studying the relationship between hypersplenism and hemodynamics in portal hypertension. It is also likely to be useful in studying the influence of diseased spleen in the treatment of portal hypertension.
MATERIAL AND METHODS: Twenty-five dogs were used randomly divided into three groups: group I (control group, n = 5), group II (PVS, n = 10) and group III (PVS + SVS, n = 10). Portal vein stenosis (PVS) was performed in dogs of group II; in group III dogs the model was first prepared by PVS and additional splenic vein stenosis 3 weeks later (PVS + SVS). Portal vein pressure (PVP), length of spleen and fluctuation of hematocyte counts were measured and recorded at the appointed times. Surgery permitted visual verification of portosystemic collateral circulation. Histopathological variation of the spleen and condition of the bone marrow hyperplasia were examined to confirm the development of hypersplenism.
RESULT: Both group II and group III developed prehepatic portal hypertension; group III also presented satisfactory hypersplenism compared to the control group and group II, as documented at surgery and by hematologic and pathologic examination.
CONCLUSIONS: Based on this study, the modified model of portal hypertension (by PVS + SVS) appears appropriate when studying the relationship between hypersplenism and hemodynamics in portal hypertension. It is also likely to be useful in studying the influence of diseased spleen in the treatment of portal hypertension.