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Inflammation: a way to understanding the evolution of portal hypertension

DOI: 10.1186/1742-4682-4-44

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Abstract:

Splanchnic and/or systemic responses to portal hypertension could have pathophysiological mechanisms similar to those involved in the post-traumatic inflammatory response.The splanchnic and systemic impairments produced throughout the evolution of experimental prehepatic portal hypertension could be considered to have an inflammatory origin. In portal vein ligated rats, portal hypertensive enteropathy, hepatic steatosis and portal hypertensive encephalopathy show phenotypes during their development that can be considered inflammatory, such as: ischemia-reperfusion (vasodilatory response), infiltration by inflammatory cells (mast cells) and bacteria (intestinal translocation of endotoxins and bacteria) and lastly, angiogenesis. Similar inflammatory phenotypes, worsened by chronic liver disease (with anti-oxidant and anti-enzymatic ability reduction) characterize the evolution of portal hypertension and its complications (hepatorenal syndrome, ascites and esophageal variceal hemorrhage) in humans.Low-grade inflammation, related to prehepatic portal hypertension, switches to high-grade inflammation with the development of severe and life-threatening complications when associated with chronic liver disease.Portal hypertension is a clinical syndrome defined by a pathological elevation of blood pressure in the portal system [1-3]. It manifests clinically as ascites, portosystemic encephalopathy and variceal hemorrhage, and often leads to death [4].Nowadays, a fundamental objective of both experimental and clinical research is the knowledge of the molecular mechanisms underlying this complex syndrome. However, the integration of these pathophysiological mechanisms in trying to understand their possible meaning is also of great interest.Knowing the final meaning of the alterations associated with portal hypertension could help to understand the meaning of the mechanisms involved in its production and maintenance. Therefore, it would be justified to speculate about the hypot

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