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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

Acute-on-chronic splanchnic inflammation. Worsening of the portal hypertensive syndrome is associated with ascites. The ascitic fluid increases the lymphatic mesenteric flow as well as the lymphatic capillary stasis in the interstitium, which in turn would worsen the splanchnic inflammatory response. GII: Gastrointestinal interstitium; HI: Hepatic interstitium; MLN: Mesenteric lymph nodes; P: peritoneum.
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Related In: Results  -  Collection


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fig3: Acute-on-chronic splanchnic inflammation. Worsening of the portal hypertensive syndrome is associated with ascites. The ascitic fluid increases the lymphatic mesenteric flow as well as the lymphatic capillary stasis in the interstitium, which in turn would worsen the splanchnic inflammatory response. GII: Gastrointestinal interstitium; HI: Hepatic interstitium; MLN: Mesenteric lymph nodes; P: peritoneum.

Mentions: Hepatic dysfunction related to fibrosis or cirrhosis would aggravate the grade of systemic inflammation characteristic of PH and as a result would increase the incidence of complications [1, 2]. Consequently, the vascular dysfunction or hyperdynamic systemic and splanchnic circulation, with increased mesenteric blood flow and portal pressure, would get worse, and interstitial hepatointestinal lymph flow would be favored. Splanchnic ischemia-reperfusion injury secondary to the acute vascular dysfunction could result in higher RAAS activity and excessive interstitial edema [47, 54, 95, 96]. The liver has been assumed to be the likely source of ascites in patients with liver disease [41]. Nevertheless, the cirrhotic liver is not the sole or even the major source of ascites in most patients [47, 54]. Weeping of fluid in great excess from the peritoneal lining and serosal surfaces of the bowel is often striking in PH as are dilated lymphatics on the surface of the small intestine, in the mesentery and within the retroperitoneal space [54]. Therefore, it is accepted that when lymphatic drainage mechanisms are overwhelmed, excess lymph is collected in the peritoneal cavity, thus causing ascites [50, 97, 98] (Figure 3). In summary, when PH is associated with severe liver disease, a higher decompensation of the splanchnic lymphatic system is induced since the lymphatic vessels' dilation plus the lymphangiogenesis do not have enough ability for draining the excessive lymph. The final consequence is the spilling of the remaining lymph into the peritoneal cavity with ascites which indeed in some cases does not have an efficient treatment.


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)

Acute-on-chronic splanchnic inflammation. Worsening of the portal hypertensive syndrome is associated with ascites. The ascitic fluid increases the lymphatic mesenteric flow as well as the lymphatic capillary stasis in the interstitium, which in turn would worsen the splanchnic inflammatory response. GII: Gastrointestinal interstitium; HI: Hepatic interstitium; MLN: Mesenteric lymph nodes; P: peritoneum.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig3: Acute-on-chronic splanchnic inflammation. Worsening of the portal hypertensive syndrome is associated with ascites. The ascitic fluid increases the lymphatic mesenteric flow as well as the lymphatic capillary stasis in the interstitium, which in turn would worsen the splanchnic inflammatory response. GII: Gastrointestinal interstitium; HI: Hepatic interstitium; MLN: Mesenteric lymph nodes; P: peritoneum.
Mentions: Hepatic dysfunction related to fibrosis or cirrhosis would aggravate the grade of systemic inflammation characteristic of PH and as a result would increase the incidence of complications [1, 2]. Consequently, the vascular dysfunction or hyperdynamic systemic and splanchnic circulation, with increased mesenteric blood flow and portal pressure, would get worse, and interstitial hepatointestinal lymph flow would be favored. Splanchnic ischemia-reperfusion injury secondary to the acute vascular dysfunction could result in higher RAAS activity and excessive interstitial edema [47, 54, 95, 96]. The liver has been assumed to be the likely source of ascites in patients with liver disease [41]. Nevertheless, the cirrhotic liver is not the sole or even the major source of ascites in most patients [47, 54]. Weeping of fluid in great excess from the peritoneal lining and serosal surfaces of the bowel is often striking in PH as are dilated lymphatics on the surface of the small intestine, in the mesentery and within the retroperitoneal space [54]. Therefore, it is accepted that when lymphatic drainage mechanisms are overwhelmed, excess lymph is collected in the peritoneal cavity, thus causing ascites [50, 97, 98] (Figure 3). In summary, when PH is associated with severe liver disease, a higher decompensation of the splanchnic lymphatic system is induced since the lymphatic vessels' dilation plus the lymphangiogenesis do not have enough ability for draining the excessive lymph. The final consequence is the spilling of the remaining lymph into the peritoneal cavity with ascites which indeed in some cases does not have an efficient treatment.

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