Experimental Models of Surgical Inflammation
- Maria-Angeles Aller 1
- Natalia de las Heras 1
- Natalia Arias
- Isabel Prieto
- Laureano Lorente
- Maria-Paz Nava 1
- Luis Santamaria
- Jorge-Luis Arias
- Vicente Lahera 1
- Jaime Arias 1
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1
Universidad Complutense de Madrid
info
- Jaime Arias
- Jose-Ignacio Arias
- Maria-Angeles Aller
Editorial: Bentham
ISBN: 978-1-60805-785-6, 978-1-60805-786-3
Año de publicación: 2013
Páginas: 309-343
Tipo: Capítulo de Libro
Objetivos de desarrollo sostenible
Resumen
Prehepatic portal hypertension induces a splanchnic low-grade inflammatory response that could switch to high-grade inflammation with the development of severe and life-threatening complications when associated with chronic liver disease. The extraembryonic origin of the portal system may determine the regression to an extraembryonic phenotype i.e., vitellogenic and amniotic, during the evolution of both types of portal hypertension. Thus prehepatic portal hypertension, or compensated hypertension by portal vein ligation in the rat, is associated with molecular mechanisms related to vitellogenesis, where hepatic steatosis and splanchnic angiogenesis stand out. In turn, extrahepatic cholestasis in the rat induces intrahepatic portal hypertension, or decompensated hypertension, with ascites and hepatorenal syndrome. The splanchnic interstitium, the mesenteric lymphatic system, and the peritoneal mesothelium seem to create an inflammatory pathway that could have a key pathophysiological relevance in the production of ascites. The hypothetical comparison between the ascitic and the amniotic fluid also allows for translational investigation. The induced regression of the splanchnic system to extraembryonic functions by portal hypertension highlights the great relevance of the extraembryonic structures even during post-natal life.