title: Experimental colitis in rats with portal hypertension and liver disease.
abstract: Within the colonic mucosa of rats with portal hypertension and liver cirrhosis, there is an increased generation of inflammatory mediators, such as leukotriene B4 and endothelin-1, and increased generation of nitric oxide. Nitric oxide overproduction may induce tissue injury. This study was undertaken to assess whether the colonic mucosa of rats with portal hypertension and liver disease have increased susceptibility to damage by noxious agents. In this study, acetic acid colitis was induced in rats with portal vein ligation and in control groups, and iodoacetamide colitis was induced in rats with partial portal vein ligation and cirrhosis due to bile duct ligation and in control groups. Rats with acetic acid colitis and those with iodoacetamide-induced colitis were studied 24 and 72 hours, respectively, after induction of colitis. Portal hypertension alone and portal hypertension with cirrhosis were present in the portal vein ligation and bile duct ligation models, respectively. In the rats with acetic acid, colitis lesion area, colonic mucosal myeloperoxidase activity, and prostaglandin E2 generation were not different between the portal vein ligation groups with and without colitis. Nitric oxide activity was higher only in the groups with colitis, irrespective of the presence of portal hypertension. In the group of rats with iodoacetamide colitis, colonic lesion area and colonic mucosal myeloperoxidase activity were similar in all groups with colitis. Colonic mucosal prostaglandin E2 generation was lower in the portal vein ligation and bile duct ligation rats with colitis compared with a control group. We concluded that rats with experimental portal hypertension do not have increased damage when induced by either acetic acid or iodoacetamide.
authors.affiliation: Department of Medicine, Hadassah University Hospital, Mount Scopus, Jerusalem, Israel. zackerman@hadassah.org.il
authors.forename: Zvi
authors.initials: Z
authors.lastname: Ackerman
authors.forename: Fanny
authors.initials: F
authors.lastname: Karmeli
authors.forename: Patrizia
authors.initials: P
authors.lastname: Cohen
authors.forename: Daniel
authors.initials: D
authors.lastname: Rachmilewitz
mesh_terms: D000477:Alkylating Agents / Q000009:adverse effects; D000596:Amino Acids / Q000009:adverse effects; D000818:Animals; D001652:Bile Ducts / Q000473:pathology / Q000503:physiopathology / Q000601:surgery; D003092:Colitis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D006439:Hemodynamics / Q000502:physiology; D006975:Hypertension, Portal / Q000150:complications* / Q000473:pathology / Q000503:physiopathology*; D007413:Intestinal Mucosa / Q000473:pathology / Q000503:physiopathology*; D007460:Iodoacetamide / Q000009:adverse effects; D008026:Ligation / Q000009:adverse effects; D008106:Liver Cirrhosis, Experimental / Q000150:complications* / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D011169:Portal Vein / Q000473:pathology / Q000503:physiopathology / Q000601:surgery; D051381:Rats; D017207:Rats, Sprague-Dawley; D012307:Risk Factors
chemical_list: D000477:Alkylating Agents; D000596:Amino Acids; D007460:Iodoacetamide