I have not any experience in this topic, however I think by ligation of portal vein or use of high dose acetaminophen or ccl4 cirrhosis and portal hypertension could be produced.
I have no experience as well in experimental model of creating EV.
I had been failed many times in creating mouse CCl4 model of cirrhosis.
Considering the splanchnic hyperdynamic state theory of the portal hypertension, may be creating an A-V fistulation on the veins draining to the esophagus with disconnection of its branches toward the liver is approachable in swine.
Two cases of esophageal varix caused by local hyperdynamic state of gastric arteries. Chang YC , Nagasue N , Kohno H , Mitsumoto Y , Yamaguchi M. Hepato-gastroenterology [1999, 46(27):1774-1777]
Abstract
With increasing evidence on the role of endogenous nitric oxide in the splanchnic hyperdynamics, the existence of esophageal varix induced by hepatopetal flow of portal hypertension in a cirrhotic patient has become more convincing. Herein, we report 2 cases of esophageal varix caused by local hyperdynamic states of the right, left and posterior gastric arteries, respectively. Angiographic evidence suggests the existence of forward flows via the submucosal A-V shunt of the gastric arteries as the etiologic causes of the varices. The treatment of the current cases was unsatisfactory due to improper recognition of the local hyperdynamic state before the treatment. Unlike the "backward flow"-type esophageal varix, the treatment strategies of the "forward flow"-type esophageal varix of hyperdynamic state caused by splanchnic A-V shunts should be considered differently.