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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

Comparative and schematic view of the amniotic egg and ascites in the decompensated portal hypertensive syndrome. Amniotic fluid circulates through the gastrointestinal tract of the embryo favoring its trophism and maturation. On the contrary, in the adult organism the proposed equivalent fluid, the ascitic fluid, is confined within peritoneal cavity. E: embryo; YS: yolk sac; I: intestine; L: liver.
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fig8: Comparative and schematic view of the amniotic egg and ascites in the decompensated portal hypertensive syndrome. Amniotic fluid circulates through the gastrointestinal tract of the embryo favoring its trophism and maturation. On the contrary, in the adult organism the proposed equivalent fluid, the ascitic fluid, is confined within peritoneal cavity. E: embryo; YS: yolk sac; I: intestine; L: liver.

Mentions: At the early stages of pregnancy, amniotic fluid consists of a filtrate of maternal blood [151, 154]. That is why drugs taken by the mother can enter amniotic fluid by diffusion across the placenta during this period [151, 155]. However, its composition is known to change as pregnancy proceeds [149]. At these stages, amniotic fluid is a bioactive medium actively secreted by the cells lining the amniotic cavity, and as gestation progresses it includes significant volume of fetal urine [156]. The hypothetical comparison of the characteristics of amniotic and ascitic fluids would oblige raising again the role of peritoneal mesothelial cells in the etiopathogeny of ascites that occurs in the portal hypertensive syndrome (Figure 8). The first fluid to enter the gastrointestinal system is amniotic fluid, and it contributes to fetal nutritional requirements and plays a significant role in gut development and maturation [156]. Thus, growth-promoting effects of amniotic fluid are equivalent to human milk [156]. The trophic effect of orally consumed amniotic fluid is attributed in part to its content in growth factors, including epidermal growth factor (EGF), hepatocyte growth factor (HGF), transforming growth factor-alpha (TGF-α), fibroblast growth factor (FGF), insulin-like growth factor (IGF-s), and VEGF [156, 157].


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)

Comparative and schematic view of the amniotic egg and ascites in the decompensated portal hypertensive syndrome. Amniotic fluid circulates through the gastrointestinal tract of the embryo favoring its trophism and maturation. On the contrary, in the adult organism the proposed equivalent fluid, the ascitic fluid, is confined within peritoneal cavity. E: embryo; YS: yolk sac; I: intestine; L: liver.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig8: Comparative and schematic view of the amniotic egg and ascites in the decompensated portal hypertensive syndrome. Amniotic fluid circulates through the gastrointestinal tract of the embryo favoring its trophism and maturation. On the contrary, in the adult organism the proposed equivalent fluid, the ascitic fluid, is confined within peritoneal cavity. E: embryo; YS: yolk sac; I: intestine; L: liver.
Mentions: At the early stages of pregnancy, amniotic fluid consists of a filtrate of maternal blood [151, 154]. That is why drugs taken by the mother can enter amniotic fluid by diffusion across the placenta during this period [151, 155]. However, its composition is known to change as pregnancy proceeds [149]. At these stages, amniotic fluid is a bioactive medium actively secreted by the cells lining the amniotic cavity, and as gestation progresses it includes significant volume of fetal urine [156]. The hypothetical comparison of the characteristics of amniotic and ascitic fluids would oblige raising again the role of peritoneal mesothelial cells in the etiopathogeny of ascites that occurs in the portal hypertensive syndrome (Figure 8). The first fluid to enter the gastrointestinal system is amniotic fluid, and it contributes to fetal nutritional requirements and plays a significant role in gut development and maturation [156]. Thus, growth-promoting effects of amniotic fluid are equivalent to human milk [156]. The trophic effect of orally consumed amniotic fluid is attributed in part to its content in growth factors, including epidermal growth factor (EGF), hepatocyte growth factor (HGF), transforming growth factor-alpha (TGF-α), fibroblast growth factor (FGF), insulin-like growth factor (IGF-s), and VEGF [156, 157].

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