A rabbit model of non-cirrhotic portal hypertension by repeated injections of E.coli through indwelling cannulation of the gastrosplenic vein.

BACKGROUND

Non-cirrhotic portal hypertension is a common cause of portal hypertension in developing countries. To understand its etiopathogenesis we developed an animal model by repeated portal endotoxemia induced through the gastrosplenic vein.

METHODS

Twenty-nine rabbits (1.5-2.0 kg) were divided into control (group I, n=13) and experimental (group II, n=16) groups. Heat killed E.coli were injected through an indwelling cannula into the gastrosplenic vein in pre-sensitized animals. The animals were sacrificed at 1, 3 and 6 months.

RESULTS

The mean portal pressure in group II animals was significantly (P<0.05) higher than in group I at 1 (17.5+/-3.4 vs 10.4+/-2.2 mmHg), 3 (17.8+/-1.3 vs 7.2+/-3.6 mm Hg), and 6 (19.8+/-3.1 vs 10.3+/-4.8 mmHg) months. Similarly, the mean splenic weight in group II was significantly greater than in group I (P<0.05). Histopathologically, the spleen showed medullary congestion, hemosidrin-laden macrophages and mild fibrosis. Histologically, the liver had normal parenchyma with mild portal lymphocytic infiltrates and kupffer cell hyperplasia. No significant anomalies were detected by liver function tests.

CONCLUSIONS

The rabbit model showed significant splenomegaly with a persistent increase in portal pressure and mild fibrosis without hepatic parenchymal injury, quite akin to non-cirrhotic portal fibrosis as seen in humans. Recurrent intra-abdominal infection may play an important role in the pathogenesis of non-cirrhotic portal fibrosis.