TOWARD A BETTER UNDERSTANDING OF PORTAL HYPERTENSIVE GASTROPATHY: THE SEARCH FOR AN IDEAL LABORATORY ANIMAL MODEL

Albillos and colleagues reported their efforts to study the evolution of the gastric microvascular changes in portal hypertension and to develop an improved animal model which more closely mimics the human form of this disorder. Using a rat model, changes in gastric mucosal microvasculature and blood flow were measured at specific stages: intervals of 1, 2, 3, 4, and 15 days after induction of portal hypertension or sham operation. Prehepatic portal hypertension was induced by partial portal vein constriction in 83 animals. In 60 animals, a sham operation was performed involving portal vein exposure. Two experimental groups were used for gastric morphometric analysis or gastric hemodynamic studies. For hemodynamic studies, a radioactive microsphere technique was used. The morphometric analysis was made from 0.5‐cm strips of gastric wall extending from the forestomach to the pylorus. An effort was made to perform the morphometric analysis at the same level within the upper oxyntic mucosa, using microphotographs and a digitized pen connected to a Zeiss videoplan‐2 image system. Noticeable changes developed in the mucosal microvasculature on day 2 after constriction of the portal vein. Gastric blood flow was decreased, and the gastric mucosal vessels had a distended lumen with a thin wall. On day 4, the gastric blood flow of the portal hypertensive animals was increased, and the mucosal vessels had a reduced lumen with thickened walls. By the 15th day, gastric blood flow remained significantly increased. The portal hypertensive animals had the largest mucosal vessel lumens and the thinnest walls. The authors concluded that the gastric mucosal vessel in the 15‐day portal vein ligated rat resembled the structural abnormalities more commonly described in human portal hypertensive gastropathy. The longer period of portal hypertension allowed and the identification of the progressive changes occurring within the microvasculature during this longer period were thought to more accurately duplicate human microvascular ahnormalities. These flndings were in contradistinction to the vascular ahnormalities produced in the two‐stage portal hypertensive animal model at 5 days used by Tarnawski et al. (1). In this earlier model, the microvascular abnormalities were characterized by thickened vessel walls and reduced lumens, flndings that were encountered on day 4 of Alhillos' study.