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The interstitial lymphatic peritoneal mesothelium axis in portal hypertensive ascites: when in danger, go back to the sea.

Aller MA, Prieto I, Argudo S, de Vicente F, Santamaría L, de Miguel MP, Arias JL, Arias J - Int J Inflam (2010)

Bottom Line: Associated liver disease increases intestinal bacterial translocation, splanchnic lymph flow, and induces ascites and hepatorenal syndrome.From a phylogenetic point of view, the ancestral mechanisms for amniotic fluid production were essential for animal survival out of the aquatic environment.However, their hypothetical appearance in the cirrhotic patient is considered pathological since ultimately they lead to ascites development.

View Article: PubMed Central - PubMed

Affiliation: Surgery I Department, School of Medicine, Complutense University of Madrid, 28040 Madrid, Spain.

ABSTRACT
Portal hypertension induces a splanchnic and systemic low-grade inflammatory response that could induce the expression of three phenotypes, named ischemia-reperfusion, leukocytic, and angiogenic phenotypes.During the splanchnic expression of these phenotypes, interstitial edema, increased lymph flow, and lymphangiogenesis are produced in the gastrointestinal tract. Associated liver disease increases intestinal bacterial translocation, splanchnic lymph flow, and induces ascites and hepatorenal syndrome. Extrahepatic cholestasis in the rat allows to study the worsening of the portal hypertensive syndrome when associated with chronic liver disease. The splanchnic interstitium, the mesenteric lymphatics, and the peritoneal mesothelium seem to create an inflammatory pathway that could have a key pathophysiological relevance in the production of the portal hypertension syndrome complications. The hypothetical comparison between the ascitic and the amniotic fluids allows for translational investigation. From a phylogenetic point of view, the ancestral mechanisms for amniotic fluid production were essential for animal survival out of the aquatic environment. However, their hypothetical appearance in the cirrhotic patient is considered pathological since ultimately they lead to ascites development. But, the adult human being would take advantage of the potential beneficial effects of this "amniotic-like fluid" to manage the interstitial fluids without adverse effects when chronic liver disease aggravates.

No MeSH data available.


Related in: MedlinePlus

Liver and spleen in a sham-operated rat (a) and in a microsurgical extrahepatic cholestatic rat (b).
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Related In: Results  -  Collection


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fig4: Liver and spleen in a sham-operated rat (a) and in a microsurgical extrahepatic cholestatic rat (b).

Mentions: To avoid these infectious complications, we have proposed performing a microsurgical technique which consists of the resection of the extrahepatic biliary tract [102, 103, 105]. The use of broad-spectrum antibiotics and vitamin K allows the long-term evolution of the rats [102, 103]. In the long-term evolution (8 to 10 weeks), microsurgical extrahepatic cholestatic rats develop hepatomegaly with a marked ductular proliferation and fibrosis [106] (Figure 4). It has been suggested that liver fibrogenesis resembles a wound-healing process leading to scar formation [107, 108]. The persistence of this inflammatory response through a longer evolution induces an “atypical” ductular proliferation with the development of a neuroendocrine compartment [109] (Figure 5). In relation to extrahepatic alterations, jaundice, choluria, PH with an enlarged spleen and collateral portosystemic circulation, hepatic encephalopathy, and ascites stand out [103, 110, 111]. Therefore, experimental extrahepatic cholestasis is a good model not only for studying chronic hepatic disease related to biliary obstruction, but also for studying extrahepatic complications, particularly ascites.


The interstitial lymphatic peritoneal mesothelium axis in portal hypertensive ascites: when in danger, go back to the sea.

Aller MA, Prieto I, Argudo S, de Vicente F, Santamaría L, de Miguel MP, Arias JL, Arias J - Int J Inflam (2010)

Liver and spleen in a sham-operated rat (a) and in a microsurgical extrahepatic cholestatic rat (b).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2990101&req=5

fig4: Liver and spleen in a sham-operated rat (a) and in a microsurgical extrahepatic cholestatic rat (b).
Mentions: To avoid these infectious complications, we have proposed performing a microsurgical technique which consists of the resection of the extrahepatic biliary tract [102, 103, 105]. The use of broad-spectrum antibiotics and vitamin K allows the long-term evolution of the rats [102, 103]. In the long-term evolution (8 to 10 weeks), microsurgical extrahepatic cholestatic rats develop hepatomegaly with a marked ductular proliferation and fibrosis [106] (Figure 4). It has been suggested that liver fibrogenesis resembles a wound-healing process leading to scar formation [107, 108]. The persistence of this inflammatory response through a longer evolution induces an “atypical” ductular proliferation with the development of a neuroendocrine compartment [109] (Figure 5). In relation to extrahepatic alterations, jaundice, choluria, PH with an enlarged spleen and collateral portosystemic circulation, hepatic encephalopathy, and ascites stand out [103, 110, 111]. Therefore, experimental extrahepatic cholestasis is a good model not only for studying chronic hepatic disease related to biliary obstruction, but also for studying extrahepatic complications, particularly ascites.

Bottom Line: Associated liver disease increases intestinal bacterial translocation, splanchnic lymph flow, and induces ascites and hepatorenal syndrome.From a phylogenetic point of view, the ancestral mechanisms for amniotic fluid production were essential for animal survival out of the aquatic environment.However, their hypothetical appearance in the cirrhotic patient is considered pathological since ultimately they lead to ascites development.

View Article: PubMed Central - PubMed

Affiliation: Surgery I Department, School of Medicine, Complutense University of Madrid, 28040 Madrid, Spain.

ABSTRACT
Portal hypertension induces a splanchnic and systemic low-grade inflammatory response that could induce the expression of three phenotypes, named ischemia-reperfusion, leukocytic, and angiogenic phenotypes.During the splanchnic expression of these phenotypes, interstitial edema, increased lymph flow, and lymphangiogenesis are produced in the gastrointestinal tract. Associated liver disease increases intestinal bacterial translocation, splanchnic lymph flow, and induces ascites and hepatorenal syndrome. Extrahepatic cholestasis in the rat allows to study the worsening of the portal hypertensive syndrome when associated with chronic liver disease. The splanchnic interstitium, the mesenteric lymphatics, and the peritoneal mesothelium seem to create an inflammatory pathway that could have a key pathophysiological relevance in the production of the portal hypertension syndrome complications. The hypothetical comparison between the ascitic and the amniotic fluids allows for translational investigation. From a phylogenetic point of view, the ancestral mechanisms for amniotic fluid production were essential for animal survival out of the aquatic environment. However, their hypothetical appearance in the cirrhotic patient is considered pathological since ultimately they lead to ascites development. But, the adult human being would take advantage of the potential beneficial effects of this "amniotic-like fluid" to manage the interstitial fluids without adverse effects when chronic liver disease aggravates.

No MeSH data available.


Related in: MedlinePlus