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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, SantamarĂ­a 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

Splanchnic lymphatic flow resulting from the gastrointestinal interstitium (GII) and the hepatic interstitium (HI) is drained through the mesenteric lymph node (MLN) in physiological situations.
© Copyright Policy - open-access
Related In: Results  -  Collection


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fig1: Splanchnic lymphatic flow resulting from the gastrointestinal interstitium (GII) and the hepatic interstitium (HI) is drained through the mesenteric lymph node (MLN) in physiological situations.

Mentions: Furthermore, once activated by proinflammatory mediators, mast cells migrate to mesenteric lymph nodes through mesenteric lymphatic vessels and thus induce lymph node hypertrophy [13]. The mesenteric lymph nodes are key structures involved in the gut-associated lymphoid tissue (GALT) [14]. GALT has an important function in the maintenance of the intestinal mucosal integrity as well as in the control of mucosal inflammation. In particular, increased infiltration by mast cells in the small bowel and mesenteric lymph nodes in experimental PH suggests their involvement in the development of portal hypertensive enteropathy and therefore in bacterial translocation, through the release of their multiple inflammatory mediators [10, 13] (Figure 1).


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, SantamarĂ­a L, de Miguel MP, Arias JL, Arias J - Int J Inflam (2010)

Splanchnic lymphatic flow resulting from the gastrointestinal interstitium (GII) and the hepatic interstitium (HI) is drained through the mesenteric lymph node (MLN) in physiological situations.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig1: Splanchnic lymphatic flow resulting from the gastrointestinal interstitium (GII) and the hepatic interstitium (HI) is drained through the mesenteric lymph node (MLN) in physiological situations.
Mentions: Furthermore, once activated by proinflammatory mediators, mast cells migrate to mesenteric lymph nodes through mesenteric lymphatic vessels and thus induce lymph node hypertrophy [13]. The mesenteric lymph nodes are key structures involved in the gut-associated lymphoid tissue (GALT) [14]. GALT has an important function in the maintenance of the intestinal mucosal integrity as well as in the control of mucosal inflammation. In particular, increased infiltration by mast cells in the small bowel and mesenteric lymph nodes in experimental PH suggests their involvement in the development of portal hypertensive enteropathy and therefore in bacterial translocation, through the release of their multiple inflammatory mediators [10, 13] (Figure 1).

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