tailieunhanh - Báo cáo y học: " Inflammation: a way to understanding the evolution of portal hypertension"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: "Inflammation: a way to understanding the evolution of portal hypertension | Theoretical Biology and Medical Modelling BioMed Central Open Access Review Inflammation a way to understanding the evolution of portal hypertension María-Angeles Aller1 Jorge-Luis Arias2 Arturo Cruz1 3 and Jaime Arias 1 Address 1Surgery I Department. Medical School Complutense University 28040 Madrid Spain 2Psychobiology Laboratory School of Psychology University of Oviedo Asturias Spain and 3General Surgery Department Virgen de la Luz General Hospital 16002 Cuenca Spain Email María-Angeles Aller - maaller@ Jorge-Luis Arias - jarias@ Arturo Cruz - acidoncha@ Jaime Arias - jariasp@ Corresponding author Published 13 November 2007 Received 5 June 2007 __J . . . AAA A_ Aiir A i-rA- AAr - AAA Accepted 13 November 2007 Theoretical Biology and Medical Modelling 2007 4 44 doi 1742-4682-4-44 This article is available from http content 4 1 44 2007 Aller et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Portal hypertension is a clinical syndrome that manifests as ascites portosystemic encephalopathy and variceal hemorrhage and these alterations often lead to death. Hypothesis 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 .

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