We have developed a new method for inducing portal hypertension and esophageal varices in rats-partial ligation of the portal vein after devascularization of the circumference of the left renal vein and complete ligation of the portal vein on the fifth day thereafter. Thirty rats were separated into groups of 10, control (sham operation), complete portal ligation only and complete portal ligation plus devascularization. Two weeks after the surgery, the presence of esophageal varices in rats with complete portal ligation plus devascularization was confirmed by portography and by the histological findings. The diameter (mean * SD) of the submucosal veins of the lower esophagus in the complete portal ligation plus devascularization group (219.4 & 86.6 pm) was significantly larger than that in the complete portal ligation group (99.8 f 53.4 p m ) or in the control group (30.5 2 16.6 pm) (p < 0.01). Vascular structures of the lower esophagus closely resembled those in humans with esophageal varices. This new technique is simple, rapid and reliable, and application can be made to various experimental studies on portal hypertension. (HEPATOLOGY 199 1;363-358.)
Numerous attempts to produce esophageal varices in laboratory animals have failed. In large animals such as monkeys or dogs, esophageal varices have been induced
Portal hypertension in rats with a partially ligated portal vein was reported by Chojkier and Groszmann in 1981 (5). On the tenth day after this operation, the rate of portosystemic shunting was about 83% to 89% (5, 6). In 1983, Sarfeh et al. (7) reported a model of portal hypertension in rats; it consisted of a two-stage occlusion of the portal vein. We designed a new and simple method to produce esophageal varices in rats by removing the main natural shunt related to the poor development of cephalad collateral veins.
Methods
Thirty male Sprague-Dawley rats, weighing 240 to 260 gm, were used. Ligation of the portal vein with devascularization of (1-4).