Experimental portal hypertension in the rat.
Previous attempts to produce sustained portal hypertension in experimental animals by portal venous obstruction have not been successful. Experiments were designed to study the effects of gradual portal venous occlusion plus hepatic lymphatic ligation in the rat. Adult male Lewis rats were divided into three groups: (A) nonoperated or sham-operated; (B) operated, with hepatic lymphatic ligation only; and (C) operated, with placement of a portal vein ameroid constrictor and hepatic lymphatic ligation. There were no differences noted in portal venous pressures (control 9.6 +/- 0.4 cm H2O) and portovenograms between groups A and B throughout the study. In group C there was greater than doubling of portal venous pressure by 1 wk which remained for 2 mo. Portal pressure then fell but remained elevated at greater than 30% above control values for 1 yr. Three systems of collateral circulation developed rapidly in response to this extrahepatic portal venous occlusion: (A) veins directly bridging across the occluding ameroid reestablishing hepatopetal flow which steadily increased; (B) spontaneous portosystemic shunts at the splenorenal area that occur early and then regress; and (C) retroperitoneal, paraesophageal and submucosal esophageal veins that develop late and remain stable. Quantitative assessment of the lumen size of the submucosal esophageal veins revealed a twofold increase in these veins in group B when compared to controls by 4 wk and a fivefold increase in these veins in group C by 8 wk that persisted for 1 yr. This model appears useful for studying the course and effects of extrahepatic portal hypertension and its gradual alteration by the spontaneous development of portosystemic collaterals in the rat. This model may have enough similarities to the extrahepatic portal hypertension seen in children that its use for future studies may be fruitful.