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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
Published online Nov 28, 2013. doi: 10.3748/wjg.v19.i44.7992
Splanchnic-aortic inflammatory axis in experimental portal hypertension
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
Revised: October 18, 2013
Accepted: October 19, 2013
Published online: November 28, 2013
Processing time: 197 Days and 20.1 Hours
Core Tip
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.