Experimental Models of Surgical Inflammation

  1. Maria-Angeles Aller 1
  2. Natalia de las Heras 1
  3. Natalia Arias
  4. Isabel Prieto
  5. Laureano Lorente
  6. Maria-Paz Nava 1
  7. Luis Santamaria
  8. Jorge-Luis Arias
  9. Vicente Lahera 1
  10. Jaime Arias 1
  1. 1 Universidad Complutense de Madrid

    Universidad Complutense de Madrid

    Madrid, España

    ROR 02p0gd045

Surgical Inflammation
  1. Jaime Arias
  2. Jose-Ignacio Arias
  3. Maria-Angeles Aller

Publisher: Bentham

ISBN: 978-1-60805-785-6 978-1-60805-786-3

Year of publication: 2013

Pages: 309-343

Type: Book chapter

DOI: 10.2174/9781608057856113010014 GOOGLE SCHOLAR lock_openOpen access editor


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.