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World J Gastroenterol. Nov 28, 2013; 19(44): 7992-7999
Published online Nov 28, 2013. doi: 10.3748/wjg.v19.i44.7992
Splanchnic-aortic inflammatory axis in experimental portal hypertension
Maria-Angeles Aller, Natalia de las Heras, Maria-Paz Nava, Javier Regadera, Jaime Arias, Vicente Lahera
Maria-Angeles Aller, Jaime Arias, Surgery Department, School of Medicine, Complutense University of Madrid, 28040 Madrid, Spain
Natalia de las Heras, Vicente Lahera, Department of Physiology, School of Medicine, Complutense University of Madrid, 28040 Madrid, Spain
Maria-Paz Nava, Animal Physiology II, School of Biology, Complutense University of Madrid, 28040 Madrid, Spain
Javier Regadera, Department of Histology and Neuroscience, School of Medicine, Universidad Autonoma, Madrid 28046, Spain
Author contributions: de las Heras N, Nava MP and Lahera V reviewed the cardiovascular physiology and pathology related to prehepatic portal hypertension; Regadera J reviewed the aortic pathology in experimental models of atherosclerosis; Aller MA and Arias J have integrated the knowledge about portal hypertension and inflammatory aortopathy in three progressive functional phases and wrote the final version of the manuscript.
Supported by Grants from Mutua Madrileña Medical Research Foundation, No. AP5966-2009
Correspondence to: Maria-Angeles Aller, MD, PhD, Surgery Department, School of Medicine, Complutense University of Madrid, Pza. de Ramón y Cajal s.n., 28040 Madrid, Spain. maaller@med.ucm.es
Telephone: +34-91-3941388 Fax: +34-91-3947115
Received: May 27, 2013
Revised: October 18, 2013
Accepted: October 19, 2013
Published online: November 28, 2013
Processing time: 197 Days and 20.1 Hours
Abstract

Splanchnic and systemic low-grade inflammation has been proposed to be a consequence of long-term prehepatic portal hypertension. This experimental model causes minimal alternations in the liver, thus making a more selective study possible for the pathological changes characteristic of prehepatic portal hypertension. Low-grade splanchnic inflammation after long-term triple partial portal vein ligation could be associated with liver steatosis and portal hypertensive intestinal vasculopathy. In fact, we have previously shown that prehepatic portal hypertension in the rat induces liver steatosis and changes in lipid and carbohydrate metabolism similar to those produced in chronic inflammatory conditions described in metabolic syndrome in humans. Dysbiosis and bacterial translocation in this experimental model suggest the existence of a portal hypertensive intestinal microbiome implicated in both the splanchnic and systemic alterations related to prehepatic portal hypertension. Among the systemic impairments, aortopathy characterized by oxidative stress, increased levels of proinflammatory cytokines and profibrogenic mediators stand out. In this experimental model of long-term triple portal vein ligated-rats, the abdominal aortic proinflammatory response could be attributed to oxidative stress. Thus, the increased aortic reduced-nicotinamide-adenine dinucleotide phosphate [NAD(P)H] oxidase activity could be associated with reactive oxygen species production and promote aortic inflammation. Also, oxidative stress mediated by NAD(P)H oxidase has been associated with risk factors for inflammation and atherosclerosis. The splanchnic and systemic pathology that is produced in the long term after triple partial portal vein ligation in the rat reinforces the validity of this experimental model to study the chronic low-grade inflammatory response induced by prehepatic portal hypertension.

Keywords: Portal hypertension; Inflammation; Aortopathy; Hepatic steatosis

Core tip: Triple partial portal vein ligation in the rat induces in the long term (22 mo) both splanchnic alterations, i.e., liver steatosis and portal hypertensive intestinal vasculopathy associated with a portal hypertensive microbiome, and systemic alterations, i.e., a wound-like inflammatory aortic response. These alterations support this experimental model of prehepatic portal hypertension for studying the pathophysiological mechanisms involved in the low-grade inflammatory response produced.