Alonso M J, Aller M A, Corcuera M T, Nava M P, Gömez F, Angulo A, Arias J
Pathology Department, Carlos III Hospital of Madrid, Spain.
Hepatogastroenterology. 2005 Mar-Apr;52(62):541-6.
BACKGROUND/AIMS: Homogenous evolution, with a narrow range of portal hypertension, degree of portosystemic shunt and hepatic atrophy has been described in the experimental model of prehepatic portal hypertension in the rat. However the great differences observed in the rats' liver weight could be attributed to a pathological alteration of the liver. Based on this, we performed an evolutive histological study of the liver. This study shows the existence of a progressive hepatocytic fatty infiltration.
Male Wistar rats with portal hypertension induced by triple stenosing ligation of the portal vein at 1 month (group II, n=4) and at 1 year (group IV, n=10) of postoperative evolution were used. The portal pressure, body, liver and splenic weights, types of collateral circulation and degree of mesenteric venous congestion were studied. The intracytoplasmatic lipid microvacuoles were quantified in hepatocytes with an image analyzer (software MIP/CID, Spain). The results were compared with those obtained in control rats with the same evolutive periods (Groups I and III).
The hepatic fatty infiltration in Group II (TPVS 1 month) (30.12+/-53.92 micron2) is similar to that presented by Group III (Control 1 year) (16.52+/-45.20 micron2), while there is an increase (p<0.001) in Group IV (triple portal vein stenosis 1 year) (182.03+/-371.42 micron2) in relation to the other groups studied. The progressive hepatic fatty infiltration in triple portal vein stenosis rats is associated with a decrease of portal pressure and of the incidence of liver hepatic atrophy, portosystemic collateral circulation and mesenteric venous congestion.
TPVS produces progressive hepatocytic fatty infiltration in the rat so that this prehepatic portal hypertension experimental model could also be considered as a hepatic steatosis model.
背景/目的：在大鼠肝前性门静脉高压实验模型中，已描述了门静脉高压、门体分流程度和肝萎缩范围较窄的同质演变情况。然而，大鼠肝脏重量的巨大差异可能归因于肝脏的病理改变。基于此，我们对肝脏进行了一项演变性组织学研究。该研究显示存在进行性肝细胞脂肪浸润。
使用在术后1个月（II组，n = 4）和1年（IV组，n = 10）通过门静脉三重狭窄结扎诱导门静脉高压的雄性Wistar大鼠。研究门静脉压力、体重、肝脏和脾脏重量、侧支循环类型以及肠系膜静脉充血程度。使用图像分析仪（西班牙MIP/CID软件）对肝细胞内的细胞质脂质微泡进行定量。将结果与相同演变期的对照大鼠（I组和III组）获得的结果进行比较。
II组（门静脉三重狭窄1个月）（30.12±53.92平方微米）的肝脏脂肪浸润与III组（对照1年）（16.52±45.20平方微米）相似，而IV组（门静脉三重狭窄1年）（182.03±371.42平方微米）相对于其他研究组有所增加（p<0.001）。门静脉三重狭窄大鼠的进行性肝脏脂肪浸润与门静脉压力降低以及肝萎缩、门体侧支循环和肠系膜静脉充血的发生率降低有关。
门静脉三重狭窄在大鼠中产生进行性肝细胞脂肪浸润，因此这种肝前性门静脉高压实验模型也可被视为肝脂肪变性模型。
