title: Portal hypertensive cardiovascular pathology: the rescue of ancestral survival mechanisms?
abstract: The portal system derives from the vitelline system, which is an extra-embryonic venous system. It could be suggested that this extraembryonic origin determines some of the characteristics attributed to portal hypertension, both compensated, i.e. prehepatic, and decompensated, i.e. fibrotic or cirrhotic. The experimental models most frequently used for studying both types of portal hypertension are portal vein ligation and common bile duct ligation in rats, respectively. We propose that in partial portal vein ligated rats, a low-grade inflammatory response, formed by the successive expression of three overlapping phenotypes - ischemia-reperfusion, vitellogenic-like and remodeling or gastrulation-like - is produced. The names of these inflammatory phenotypes developed in compensated portal hypertension are based on some metabolic similarities that can be established with the abovementioned phases of embryonic development. In bile-duct ligated rats, decompensation related to hepatic insufficiency would induce a high-grade inflammatory response. In this experimental model, the splanchnic interstitium, the mesenteric lymph and the peritoneal mesothelium seem to create an inflammatory axis that produces ascites. The functional comparison between the ascitic and the amniotic fluids would imply that, in the decompensated portal hypertensive syndrome, the abdominal mesothelium acquires properties of the amniotic membranes or amnion. In conclusion, the hypothetical comparison between the inflammatory portal hypertensive evolutive types and the evolutive phases of embryonic development could allow for translational research.
authors.affiliation: Department of Surgery I, School of Medicine, Complutense University of Madrid, Plaza de Ramon y Cajal s.n., 28040 Madrid, Spain.
authors.forename: Maria-Angeles
authors.initials: MA
authors.lastname: Aller
authors.forename: Natalia
authors.initials: N
authors.lastname: Heras
authors.forename: Javier
authors.initials: J
authors.lastname: Blanco-Rivero
authors.forename: Jose-Ignacio
authors.initials: JI
authors.lastname: Arias
authors.forename: Vicente
authors.initials: V
authors.lastname: Lahera
authors.forename: Gloria
authors.initials: G
authors.lastname: Balfagón
authors.forename: Jaime
authors.initials: J
authors.lastname: Arias
mesh_terms: D000653:Amniotic Fluid; D000818:Animals; D001202:Ascitic Fluid; D003135:Common Bile Duct / Q000473:pathology*; D004195:Disease Models, Animal; D006975:Hypertension, Portal / Q000276:immunology / Q000473:pathology*; D007249:Inflammation / Q000473:pathology*; D008026:Ligation; D010641:Phenotype; D011169:Portal Vein / Q000473:pathology*; D051381:Rats; D015427:Reperfusion Injury / Q000473:pathology; D014816:Vitelline Duct / Q000473:pathology