The splanchnic inflammation inchronic liver disease increases intestinal angiogenesis. In the current study our aim was demonstrating that the small bowel lymphangiogenesis is associated with angiogenesis in chronic c...The splanchnic inflammation inchronic liver disease increases intestinal angiogenesis. In the current study our aim was demonstrating that the small bowel lymphangiogenesis is associated with angiogenesis in chronic cholestasis in the rat. A stereological study of the lymphatic microcirculation in the small intestine was performed in cholestatic rats. Portal enteropathy in cholestasis increases lymphatic microvessels in the mucosa and submucosa layers. Thus, the lymphatic microvessel volume fraction was superior (p < 0.001) in the mucosa (0.16 ± 0.01) and submucosa (0.16 ± 0.01), in regard to the muscle layer 0.015 ± 0.01. The lymphatic microvessel length density was higher in the mucosa (76.89 ± 2.86 mm-2;p -2;p < 0.01), in relationship to the muscle layer (5.04 ± 2.92 mm-2). These alterations predominate in the duodenum (volume fraction: 0.10 ± 0.01 and length density: 33.55 ± 5.98 mm-2) and ileum (volume fraction: 0.16 ± 0.01 and length density: 38.62 ± 6.07 mm-2). This study demonstrates the predominance of an increased lymphangiogenic response in both end sides of the small bowel associated with chronic liver disease. Since the porto-systemic venous collateral circulation in the chronic liver insufficiency is developed in the ends of the gastrointestinal tract, the excessive duodeno-ileal lymphangiogenesis could suggest the development of amesenteric-systemic lymphatic bypass in the chronic portal hypertension.展开更多
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 c...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 maybe determines 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 extraem-bryonic structures even during postnatal life.展开更多
文摘The splanchnic inflammation inchronic liver disease increases intestinal angiogenesis. In the current study our aim was demonstrating that the small bowel lymphangiogenesis is associated with angiogenesis in chronic cholestasis in the rat. A stereological study of the lymphatic microcirculation in the small intestine was performed in cholestatic rats. Portal enteropathy in cholestasis increases lymphatic microvessels in the mucosa and submucosa layers. Thus, the lymphatic microvessel volume fraction was superior (p < 0.001) in the mucosa (0.16 ± 0.01) and submucosa (0.16 ± 0.01), in regard to the muscle layer 0.015 ± 0.01. The lymphatic microvessel length density was higher in the mucosa (76.89 ± 2.86 mm-2;p -2;p < 0.01), in relationship to the muscle layer (5.04 ± 2.92 mm-2). These alterations predominate in the duodenum (volume fraction: 0.10 ± 0.01 and length density: 33.55 ± 5.98 mm-2) and ileum (volume fraction: 0.16 ± 0.01 and length density: 38.62 ± 6.07 mm-2). This study demonstrates the predominance of an increased lymphangiogenic response in both end sides of the small bowel associated with chronic liver disease. Since the porto-systemic venous collateral circulation in the chronic liver insufficiency is developed in the ends of the gastrointestinal tract, the excessive duodeno-ileal lymphangiogenesis could suggest the development of amesenteric-systemic lymphatic bypass in the chronic portal hypertension.
文摘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 maybe determines 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 extraem-bryonic structures even during postnatal life.
